Treatment of BRAF Mutated Non-Small Cell Lung Cancer - Episode 1
Mark A. Socinski, MD: This 67-year-old female presented with some dyspnea and coughing, as well as hemoptysis. Her history was significant for some mild COPD. Because of her symptoms, her ECOG performance status was categorized as 1. She had a CT scan, because of her symptoms, that showed a 3 cm right lower lobe lesion. There was some ipsilateral mediastinal adenopathy, as well as severalin the range of 3 to 4, 2 to 2.5 cm—liver lesions on that CT scan. A core biopsy of 1 of the accessible liver lesions showed an adenocarcinoma, moderately differentiated. She did have a smoking history, about 30 packs/year of exposure, but she had quit 10 years ago.
She was appropriately tested for molecular drivers, and she had an extensive panel going beyond the standardEGFR,ALK, andROS1, and in this case, aBRAF V600Emutation was detected. We also know she was tested for PD-L1, and that was negative at the time of her diagnosis. That summarizes the case. What we have is a 67-year-old female, otherwise fit, who is a former smoker, who presents with stage 4 adenocarcinoma of the lung. She is known to have aBRAF V600Emutation. She is not PD-L1-positive. Again, this is an example of what I would consider treatable, but not curable, disease at this point.
My initial impressions of this woman are, again, that we have clarity of the diagnosis, because we have a nice core biopsy. We also know that she is not PD-L1-positive in this setting. We know that a molecular driver, aBRAF V600Emutation, was found. She has a good performance status, so I think she has a couple of options in this setting. Again, I think she has very treatable, but again, not curable, disease.
This patient’s prognosis is probably around 1 year to 14 months’ median overall survival time. One of the things we don’t have sufficient data on is how theBRAFmutation alters that prognosis. And although we have some exciting data with targeted therapy in regard to the response rates of these targeted agents, I don’t know that we have enough mature survival data. For instance, in theEGFR-mutant population, we know that having anEGFRmutation is both prognosticpatients do better with it—as well as predictive. It predicts for a better response to EGFR TKIs. I think what we know aboutBRAFmutations is that they are predictive for oral TKIs to have a higher response rate, but the impact that it has on the prognosis is not entirely clear at this point. We need some more mature data.
Transcript edited for clarity.