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  • Meeting abstract
  • Open Access

Association between [18F]-fluoro-2-deoxyglucose uptake and expressions of hypoxia-induced factor 1α and glucose transporter 1 in non-small cell lung cancer

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Journal of Cardiothoracic Surgery201510 (Suppl 1) :A211

  • Published:


  • Overall Survival
  • Adenocarcinoma
  • Squamous Cell Carcinoma
  • Glucose Transporter
  • Lung Adenocarcinoma


High maximal standardized uptake values (SUVmax) on [18F]-fluoro-2-deoxyglucose positron emission tomography (FDG-PET) are associated with inferior survival in non-small cell lung cancer (NSCLC).


Here, we investigated the biological mechanisms underlying FDG uptake in NSCLC.


This study included 133 patients with NSCLC (109 with adenocarcinoma and 24 with squamous cell carcinoma). The patients underwent tumor resection, at the latest, 4 weeks after FDG-PET. The SUVmax values for primary lesions were calculated based on FDG uptake. The expression of hypoxia-inducible factor 1α (HIF1α) and glucose transporter 1 (GLUT1) was evaluated on immunostained tumor sections using six-point grading scales.


SUVmax and the expression of HIF1α and GLUT1 were significantly higher in squamous cell carcinoma than in adenocarcinoma (p < 0.001, p = 0.034, and p < 0.001, respectively). In adenocarcinoma, but not squamous cell carcinoma, SUVmax, HIF1α, and GLUT1 correlated with various clinicopathological factors relating to malignancy, and SUVmax and GLUT1 were associated with disease-free survival (DFS) (p < 0.001 and p = 0.029) and overall survival (OS) (p < 0.001 and p = 0.033, respectively). Moreover in adenocarcinoma, HIF1α and GLUT1, GLUT1 and SUVmax, and HIF1α and SUVmax were significantly correlated (p < 0.001 for all), suggesting that HIF1α-induced GLUT1 might influence SUVmax values on FDG-PET.


In lung adenocarcinoma, but not squamous cell carcinoma, HIF1α, and GLUT1 expressions indicate tumor aggressiveness pathologically, and might explain high FDG uptake on PET and correlate with poor prognosis.

Authors’ Affiliations

Department of Surgical Oncology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan
Department of Pathology, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan


© Furukawa et al. 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.