Cancer immunotherapy biomarkers

The immune system can help protect the body against cancer by sending T cells to attack tumour cells. However, tumour cells can produce a protein called programmed death-ligand 1 (PD-L1), enabling cancers to evade the immune system.1,2

PD-L1 works like a ‘stop sign’ inactivating T cells. Interfering with PD-L1 is one way to help prevent cancer from disabling T cells in the tumour microenvironment, where tumours grow and interact with other cells.2,3

Studies are investigating whether high amounts of PD-L1 may indicate tumours more likely to respond to immunotherapies that interfere with PD-L1.2,4

As a tumour grows, many other cells join the tumour microenvironment.

These cells, called ‘tumour-infiltrating immune cells,’ can also express PD-L1 in many types of cancer. 1,2,5-7

PD-L1 on both tumour cells and tumour-infiltrating immune cells may help prevent T cells from attacking tumour cells.2,3

The role of PD-L1 on tumour cells and tumour-infiltrating immune cells is an important area of cancer immunotherapy research.

Studies are evaluating whether measuring the amount of PD-L1 on both tumour cells and tumour-infiltrating immune cells may help predict how well certain medicines may work, or whether measuring the amount of PD-L1 on tumour-infiltrating immune cells alone could be sufficient to serve the same purpose.8,9

Ongoing clinical studies are examining the significance of measuring the amount of the PD-L1 on tumour cells and tumour-infiltrating immune cells across diferent types of cancers, which could help doctors determine which people are most likely to respond to cancer immunotherapy alone or who may need a combination with other medicines.

The PD-L1/PD-1 pathway: a security checkpoint

Dr. Daniel Chen explains how immunotherapy may affect the PD-L1/PD-1 pathway, enabling the body to better detect and fight cancer.

References

  1. Chen DS, Mellman I. Immunity. 2013. 39:1-10

  2. Chen DS, et al. Clin Cancer Res. 2012. 18:6580-6587

  3. Keir ME, et al. Annu Rev Immunol. 2008. 26:677-704

  4. Quezada SA, Peggs KS. Br J Cancer. 2013. 108:1560-1565

  5. Data on file, Genentech

  6. Pardoll DM. Nat Rev Cancer. 2012. 12:252-264

  7. Sharma P, et al. Proc Natl Acad Sci USA. 2007. 104:3967-3972

  8. Herbst RS, et al. Nature. 2014. 515:563-567

  9. Powles T, et al. Nature. 2014. 515:558-562