In a recent groundbreaking study, a team of researchers led by BIDMC’s Dipak Panigrahy, MD, a scientist at the Cancer Center at BIDMC, demonstrated that dead and dying cancer cells killed by conventional cancer treatments paradoxically trigger the inflammation that promotes tumour growth and metastasis.
Now, in a follow-up study published in January in Proceedings of the National Academy of Science (PNAS), Panigrahy and colleagues illuminate the mechanism by which debris generated by ovarian tumour cells targeted by first-line chemotherapy accelerates tumour progression.
Additionally, the researchers describe a novel approach to suppressing the chemotherapy-induced tumour growth.
“Conventional cancer therapy is a double-edged sword – the very treatment meant to control cancer is also helping it to survive and grow,” said Panigrahy, Assistant Professor of Pathology in the Department of Pathology and a Scientist at the Cancer Center at BIDMC
“To prevent tumour recurrence after therapy, it will be critical to neutralise the inherent tumour-promoting activity of therapy-generated debris.”
Panigrahy and colleagues’ analysis revealed that chemotherapy-killed ovarian cancer cells induce surrounding immune cells called macrophages to release a surge of immune-related chemical compounds – cytokines and lipid mediators – that create optimal conditions in which tumours can survive and grow.
Next, the team showed that a common anti-inflammatory drug called a dual COX-2 inhibitor to block that surge of tumour-friendly cytokines and lipids.
“The role of these chemotherapy-induced cytokines and lipids is under-appreciated and poorly characterised, and ovarian cancer patients may benefit from suppressing their release,” said Panigrahy.
“Further research is needed but, dual inhibition of the COX-2 pathways is a novel therapeutic modality that may compliment conventional cancer therapies by acting as a surge protector against cell debris-stimulated tumour growth.”