Efficacy of chemoimmunotherapy in a lung adenocarcinoma patient with mutations in the KRAS and STK11

Immunotherapy is a groundbreaking treatment method when it comes to cancer, and this includes non-small-cell lung cancer (NSCLC). In NSCLC patients, immunotherapy is used in a form of immune checkpoint inhibitors (ICIs), and depending on the proportion of tumor cells with programmed death ligand 1 (PD-L1) expression on them, it can be administered either in monotherapy (≥ 50%) or in combination with chemotherapy (< 50%). In this article, we would like to present a case of a female patient with Kirsten Rat Sarcoma Virus (KRAS)-mutated lung adenocarcinoma who was responding to chemoimmunotherapy for a long time despite the presence of co-mutation in the Serine/Threonine Kinase 11 (STK11) gene, known to worsen immunotherapy outcomes. In this patient, another mutation was found — in the nibrin (NBN) gene, which is of uncertain relevance, but it presumably could be connected to a better outcome as it encodes proteins involved in DNA repair. Deficiency in DNA repair may be marked by homologous recombination deficiency (HRD), and there already exists some evidence of better immunotherapy efficacy in patients with HRD. Considering the above, further investigation and thorough genetic diagnostics in NSCLC patients are required to fully understand the background of immunotherapy response.