@article {KAIRA3775, author = {KYOICHI KAIRA and TOSHIAKI TAKAHASHI and HARUYASU MURAKAMI and TAKEHITO SHUKUYA and HIROTSUGU KENMOTSU and TATEAKI NAITO and NOBORU ORIUCHI and YOSHIKATSU KANAI and MASAHIRO ENDO and HARUHIKO KONDO and TAKASHI NAKAJIMA and NOBUYUKI YAMAMOTO}, title = {Relationship between LAT1 Expression and Response to Platinum-based Chemotherapy in Non-small Cell Lung Cancer Patients with Postoperative Recurrence}, volume = {31}, number = {11}, pages = {3775--3782}, year = {2011}, publisher = {International Institute of Anticancer Research}, abstract = {Background: The aim of this study was to investigate whether L-type amino acid transporter 1 (LAT1) expression can predict poor outcome after chemotherapy in patients with non-small cell lung cancer (NSCLC). Materials and Methods: Immunohistochemistry was carried out to examine the expression of LAT1, CD98, vascular endothelial growth factor (VEGF), Ki-67, phosphorylation of Akt (p-Akt), phosphorylation of mammalian target of rapamycin (p-mTOR) and p53 in resected lung tumor specimens obtained from 56 patients treated with platinum-based chemotherapy. Results: Positive LAT1 and CD98 expression was recognized in 45\% (25/56) and 34\% (19/56), respectively. In NSCLC (N=56), LAT1, CD98, VEGF, Ki-67 and p53 were significant factors for predicting poor outcome, and adenocarcinoma was an independent factor for predicting favorable prognosis. LAT1 expression was closely associated with chemoresistance. In adenocarcinoma (N=37), a statistically significant inverse relationship was observed between the expression of LAT1, VEGF and Ki-67 and epidermal growth factor receptor (EGFR) mutation, and positive expression of LAT1 and VEGF was an independent factor for predicting poor prognosis after chemotherapy. Conclusion: LAT1 expression may be useful for predicting response and outcome after systemic chemotherapy.}, issn = {0250-7005}, URL = {https://ar.iiarjournals.org/content/31/11/3775}, eprint = {https://ar.iiarjournals.org/content/31/11/3775.full.pdf}, journal = {Anticancer Research} }