**1. Introduction**

Pulmonary pleomorphic carcinoma (PPC) is a rare disease with an incidence of 0.1%–0.4% among all lung cancers and shows a poor prognosis because of its resistance to systemic chemotherapy [1]. PPC includes carcinomatous and sarcomatoid components and is classified as a subtype of sarcomatoid carcinoma of the lung by the World Health Organization histologic classification of lung neoplasms [2,3]. Because of its rarity and low treatment efficacy, most patients with PPC exhibit recurrence even after complete surgical resection; moreover, there are no standard treatments for patients with advanced and inoperable PPC. The development of appropriate treatments and identification of predictive biomarkers are critical for improving the prognosis of patients with complex histologies, such as PPC.

Glucose metabolism is associated with tumor progression and metastases, and is used in molecular imaging, such as 2-[18F]-fluoro-2-deoxy-d-glucose (18F-FDG) positron emission tomography (PET), to detect cancers [4]. Although there are several types of glucose transporters (GLUTs), glucose transporter 1 (GLUT1) and GLUT3 are strongly expressed on the membrane of tumor cells, and a meta-analysis demonstrated GLUT1 to be a prognostic marker for predicting worse outcomes in patients with lung cancer [4]. 18F-FDG accumulates in tumor cells via GLUT1, a process closely associated with poor prognosis and tumor progression in patients with lung cancer [5]. We previously showed that 18F-FDG uptake in PPC is closely related to the presence of GLUT1 and angiogenesis, and that the accumulation of 18F-FDG and the expression level of GLUT1 were significantly higher in patients with PPC than those with other nonsmall cell lung cancer (NSCLC) [6]. This indicates that tumor glucose metabolism involving GLUT1 plays a crucial role in the carcinogenesis of PPC. 18F-FDG-PET can be used to detect primary and metastatic lesions for disease staging in patients with PPC. From a pathological perspective, studies are needed to determine how the expression of GLUT1 in cancer-specific glucose metabolism reflects the survival and metastasis of patients with PPC. However, little is known about the clinicopathological relevance of GLUT1 expression in patients with PPC.

In this clinicopathological study, we examined the prognostic role of GLUT1 expression in patients with surgically resected PPC.
