Send to

Choose Destination
See comment in PubMed Commons below
Lung Cancer. 2009 Oct;66(1):120-6. doi: 10.1016/j.lungcan.2008.12.015. Epub 2009 Jan 26.

Prognostic significance of L-type amino acid transporter 1 (LAT1) and 4F2 heavy chain (CD98) expression in stage I pulmonary adenocarcinoma.

Author information

  • 1Department of Medicine and Molecular Science, Gunma University Graduate School of Medicine, Showa-machi, Maebashi, Gunma 371-8511, Japan.



The purpose of this study was to evaluate the prognostic value of l-type amino acid transporter 1 (LAT1) and 4F2 heavy chain (CD98) expression in patients with stage I pulmonary adenocarcinoma.


A total of 139 consecutive patients with pathologic stage I pulmonary adenocarcinoma were retrospectively reviewed. Expression of LAT1, CD98, Ki-67 labeling index, vascular endothelial growth factor (VEGF) and microvessel density (MVD) was also evaluated immunohistochemically and correlated with the prognosis of patients after complete resection of the tumor.


LAT1 and CD98 expression were positive in 23% (32/139) and 22% (31/139), respectively (p=0.887). LAT1 with CD98 expression was recognized in 15% (21/139). LAT1 expression was significantly correlated with CD98, Ki-67 labeling index, VEGF, and MVD. The 5-year survival rates of LAT1-positive and -negative patients and CD98-positive and -negative patients, were 60.2 and 95.2% (p<0.0001) and 72.5 and 93.4% (p=0.0008), respectively. Univariate analysis disclosed that cellular proliferation and MVD in the tumor were significant prognostic factors. However, multivariate analysis confirmed that positive expression of LAT1 and CD98 was an independent factor for predicting a poor prognosis.


The overexpression of LAT1 and CD98 is a pathological factor to predict the prognosis in patients with resectable stage I pulmonary adenocarcinoma.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center