Deep and Prolonged Response to Aurora A Kinase Inhibitor andSubsequently to Nivolumab in MYCL1-Driven Small-Cell LungCancer: Case Report and Literature Review

Small-cell lung carcinoma (SCLC) is one of the most aggressive solid tumors, and the prognosis has not improved significantly in25 years. Despite a recent understanding of the genomic aberrations seen in SCLC, these insights have not led to any breakthroughsin treatment. We present a patient with SCLC harboring a novel MYCL1 fusion protein who experienced a prolonged diseasecourse due to the use of Aurora A kinase inhibitor and subsequently nivolumab. MYC family genes are master regulators ofseveral cellular pathways including proliferation, differentiation, and apoptosis and recently have been shown to be involvedin tumor immune evasion. Large studies have shown that a significant proportion of patients with SCLC haveamplification or overexpression of MYC family genes. Preclinical data have exposed vulnerability of MYC-driven tumors toAurora kinase inhibitors, bromodomain and extraterminal domain inhibitors, and recently to immune checkpoint blockers.Further studies using these agents with selective enrolling of patients with MYC-altered tumors are warranted to exploitthese vulnerabilities.