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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.<sup>1,2</sup>

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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

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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

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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

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

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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

Decorative illustration of cancer immunotherapy

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