Cancer Research UK-funded scientists from the University of Sheffield found that the cancer-killing action of chemotherapy can trigger a swarm of wound-healing, white blood cells to cluster around blood vessels in a treatment-hit tumour. These cells – called M2 macrophages – repair tissue damage and build new blood vessels, a process that sometimes helps the tumour to grow again after treatment.
But by treating mice with cancer with a drug that stops these repair cells from working, the researchers markedly reduced the speed at which tumours grew back after chemotherapy.
The lead scientist on the study, Professor Claire Lewis at the University of Sheffield’s Department of Oncology, said: “Scientists already knew that the body’s drive to heal itself can sometimes backfire when the immune system reacts to tissue damage. Our research shows that treating tumours with chemotherapy can activate this part of the immune system, and this then helps tumours re-grow afterwards.”
“But combining chemotherapy with a drug that switches off this part of the body’s repair system, slowed the growth of tumours after chemotherapy. This could be particularly important for patients who can’t have surgery and, therefore, need chemotherapy to help them live for as long as possible.“
Dr Áine McCarthy, science communications officer at Cancer Research UK, said: “Chemotherapy is a cornerstone cancer treatment that saves thousands of lives, but sometimes tumours come back, reducing patients’ chances of survival. We don’t understand all the reasons why tumours do come back, but this study sheds new light on the role of the immune system in causing tumours to grow again and, importantly, identifies a drug that could block this happening if given at the same time as chemotherapy.”
“But this is early research carried out in mice and more work is needed to see if blocking M2 macrophages can also slow down tumour re-growth in patients.”
Hughes et al. Perivascular M2 macrophages stimulate tumour relapse after chemotherapy. Cancer Res., 2015; DOI: 10.1158/0008-5472.CAN-14-3587 [Abstract]