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Hide, Seek, Treat: Outsmarting Gestational Trophoblastic Neoplasia with Immunotherapy
Gestational trophoblastic neoplasia (GTN) (a form of Gestational Trophoblastic Disease) is a type of malignant (cancerous) tumour that develops during or after pregnancy from cells that would normally form the placenta – the organ that feeds the growing baby. GTN is rare and also highly unusual. Whilst all other cancers grow from the body’s own cells, GTN comes from cells that belong to the placenta which genetically is part of the fetus.
Usually, cells in the body that aren’t ‘self’ are recognised as foreign & destroyed by the immune system. However, special mechanisms come in to play during pregnancy, which limits immune reactions to prevent the mother’s immune system destroying the baby and placenta. As is typical of cancers, however, GTN can hijack these mechanisms to avoid being targeted by the immune system, enabling it to grow and spread to other parts of the mother’s body.
On the flip side, GTN responds much better than other cancers to a certain type of immunotherapy, with a cure rate of around 75%. Immunotherapy works by stimulating the body’s own immune system to target and kill cancer cells, which begs the obvious question: how does this treatment expose the tumour to attack by the immune system?
This is precisely the topic that Yiming Guan, a PhD student funded by the Cancer Treatment & Research Trust, is researching. Together with his coworkers, and under the supervision of Dr Ehsan Ghorani, Yiming aims to investigate the immune cell ‘landscape’ of GTN, in essence creating a directory of the types and locations of immune cells around the tumour before and after immunotherapy. The current thinking is that, in the absence of immunotherapy, GTN tumour cells send instructions to a certain type of immune cell (a CD4 T cell), telling it to adopt a more tolerant role and to talk its comrades out of mounting an immune attack; immunotherapy, however, intercepts these messages so that CD4 cells enlist in and coordinate an immune cell army to destroy the tumour cells. Precisely what determines whether these T cells behave as peacekeepers or soldiers, though, isn’t fully understood.
In the 3-year PhD project funded by CTRT, Yiming and his fellow lab mates will use state-of-the-art ‘multi-omics’ techniques to generate huge amounts of information about the biological molecules that are present in GTN tumours, and immune cells from tissue samples taken from untreated patients and from patients given the immunotherapy drug Pembrolizumab. Changes in the amounts of particular molecules and/or their whereabouts within individual tumour and immune cells could give us more insight into the mechanisms that militarize T cells against the tumours.
Since GTN responds so well to immunotherapy, these studies could uncover important principles that might help to improve this treatment for other, more common cancers that do not usually respond well to treatment.
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