Promising results from a clinical trial show more patients with advanced non-small-cell lung cancer could benefit from the immunotherapy drug pembrolizumab. In the trial, compared with chemotherapy, the immunotherapy drug improved survival in all patients whose tumors express a protein called PD-L1.

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The researchers say the trial results give further support for broadening availability of pembrolizumab for all advanced NSCLC patients with PD-L1 expression over 1%.

Results from the phase 2/3 trial – published in The Lancet – were presented at the first European Society for Medical Oncology (ESMO) Asia Congress in Singapore earlier this week.

An immunotherapy cancer drug works by getting the immune system to fight the cancer. Pembrolizumab (brand name Keytruda), is already approved by the Food and Drug Administration (FDA) for the treatment of certain categories of advanced non-small-cell lung cancer (NSCLC) and advanced melanoma.

Pembrolizumab is an antibody drug that targets a cellular pathway called PD-1/PD-L1. PD-1 is a receptor, and PD-L1 is one of the molecules that binds to it. The pathway is an example of what is called an immune checkpoint.

Many cancers are able to avoid attack from a patient’s immune system by overriding their “immune checkpoints” – molecules on immune cells that need to be activated or silenced to start an immune response.

By blocking the PD-1/PD-L1 pathway, pembrolizumab may boost the immune system’s ability to fight the cancer cells.

Pembrolizumab is shown to be effective against various types of cancer, including melanoma and lung cancer, where it has shown durable anti-tumor activity and acceptable toxicity in previously treated and untreated patients with advanced NSCLC.

The new trial is the first to assess the effectiveness of the immunotherapy drug as a second or later line treatment in advanced NSCLC patients positive for PD-L1.

The trial – called KEYNOTE-010 – tested two doses of pembrolizumab against the commonly used chemotherapy drug docetaxel in patients with tumors expressing PD-L1.

The results showed that both doses – the FDA-approved 2 mg/kg dose and an investigational 10 mg/kg dose, each given every 3 weeks – improved median survival in all PD-L1-positive patients, compared with chemotherapy.

The researchers note that the benefit is even greater in the group of patients with 50% or more of tumor cells expressing PD-L1.

Trial leader Roy Herbst, professor of medicine and pharmacology and chief of Medical Oncology, Yale Cancer Center at Yale School of Medicine in New Haven, CT, says:

The topline results show that both groups of patients receiving pembrolizumab experience a survival benefit compared to docetaxel.”

The trial, which took place from August 2013-August 2015, enrolled 1,034 patients from 24 countries from Europe, the US and Asia (including Japan, South Korea and Taiwan). They were randomly assigned to receive either immunotherapy or chemotherapy.

All patients had experienced disease progression following platinum-containing systemic therapy and were categorized by PD-L1 expression (expressed in 1-49% tumors, and expressed in 50% or more of tumors).

Prof. Herbst says that – as expected – the results were even better for patients with higher tumor expression of PD-L1, and treatment with pembrolizumab was associated with longer overall survival compared with chemotherapy (median overall survival of 14.9 and 17.3 months with 2 mg/kg and 10 mg/kg of pembrolizumab compared with 8.2 months with chemotherapy).

He says the trial also shows there is a clear benefit in patients with over 1% PD-L1 tumor expression score and concludes:

These results give further support for broadening the availability of pembrolizumab for all patients with PD-L1 expression over 1%.”

The researchers note that further studies are needed to find out if patients who express PD-L1 in less than 1% of tumor cells might benefit from pembrolizumab.

Another study that Medical News Today reported earlier this year covered the discovery of a molecular mechanism that allows tumors to develop resistance to chemotherapy. The mechanism acts as a backup when a gene called p53, which normally helps healthy cells prevent mutations, is missing.