Dr. Jack West reviews the concept of epigenetics, epigenetic priming, and whether oral azacytidine can improve outcomes in patients who receive immunotherapy for advanced lung cancer.

Drs. Leora Horn, Ben Solomon, & Jack West assess whether clinical factors such as being a never-smoker or having a driver mutation (EGFR, ALK, etc.) reliably predict minimal benefit from immunotherapy agents.

Dr. Eddie Garon, UCLA, reviews the controversial question of whether PD-L1 expression is a reliable enough biomarker to be used to select patients to receive or not receive immune checkpoint inhibitor therapy in lung cancer.

Drs. Leora Horn, Ben Solomon, & Jack West consider the factors that might lead us to favor testing for PD-L1 at initial workup of a patient with advanced NSCLC or after progression.

Immune checkpoint inhibitors are now becoming approved and commercially available for patients with previously treated advanced NSCLC. Dr. Eddie Garon, medical oncologist at UCLA, summarizes key data and explains their current role in treatment.

Drs. Ben Solomon, Leora Horn, & Jack West consider how valuable testing for PD-L1 expression is in clinical practice and whether it should be integrated in clinical decision making around immunotherapies.

Dr. Eddie Garon from UCLA Medical Center reviews the general mechanism of action of immune checkpoint inhibitors and how they can be an effective therapy in lung cancer.

The current standard of care for SCLC shows limited results with high toxicities. Drs. Soria, Gandhi, and West discuss new ASCO 2015 data that show promise for a subset of patients with PD-L1 expression on Keytruda (pembrolizumab) or Opdivo (nivolumab).

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As more immunotherapeutics become available to treat lung cancer, research must determine how to balance efficacy, toxicities, and cost. That means finding which patients who will benefit from which drugs while maintaining good quality of life.

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Novel immunotherapy agent atezolizumab (MPDL3280A) looks superior to Taxotere (docetaxel) in a study, specifically for patients with PD-L1. What are the implications of multiple agents with similar mechanisms of action in the same clinical settings?

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