High co-expression of PD-L1 and HIF-1α correlates with tumour necrosis in pulmonary pleomorphic carcinoma

摘要: Abstract Background Pulmonary pleomorphic carcinomas (PPCs) are uncommon malignant tumours characterised by an aggressive clinical course and poor survival. These neoplasms frequently exhibit marked confluent necrosis, in which hypoxia levels extremely high, causing low responsiveness to chemotherapy conferring basic resistance anti-cancer drugs. Programmed death ligand 1 (PD-L1)–mediated immune escape may be underlying source of a suitable target for specific therapy, but its role PPCs is unclear. Materials methods In total, 122 were investigated. Paraffin-embedded tumour sections stained with PD-L1 hypoxia-inducible factor-1α (HIF-1α) antibodies. Overexpression was denoted moderate-to-strong membrane staining ≥5% cells HIF-1α nuclear ≥10% cells. The presence driver mutations the epidermal growth factor receptor ( EGFR ), Kirsten rat sarcoma viral oncogene homolog KRAS v-raf murine B BRAF telomerase reverse harscriptase gene TERT phosphoinositide 3-kinase catalytic alpha PIK3CA anaplastic lymphoma kinase ALK ROS1 (ROS1 proto-oncogene tyrosine kinase) genes examined. Results overall frequencies overexpression mutation 70.5, 75.4, 22.1%, respectively. High expression significantly correlated that p  = 0.015). Advanced stage high two independent risks Conclusions co-expression observed compared their conventional non-small-cell lung carcinoma. behaviour PPC could partially related PD-L1–mediated intratumoural hypoxia. correlates prognosis provide rationale use targeted immunotherapy this subtype high-grade PPC.