title: CD26 overexpression is associated with prolonged survival and enhanced chemosensitivity in malignant pleural mesothelioma.
abstract: OBJECTIVE
  Malignant pleural mesothelioma (MPM) is an aggressive and therapy-resistant neoplasm arising from the pleural mesothelial cells, without established indicators to predict responsiveness to chemotherapy.
  
  
  METHODS
  Our study involving 79 MPM patients showed that 73.4% of MPM expressed CD26 on cell membrane.
  
  
  RESULTS
  The majority of epithelioid and biphasic types of MPM expressed CD26 on the cell membrane, whereas the sarcomatoid type showed a lack of CD26 surface expression. Although the sarcomatoid type was associated with poor prognosis (P < 0.0001), no significant relationship between CD26 expression and survival was observed. On the contrary, there was a trend for an association between response rate to chemotherapy and CD26 expression (P = 0.053), with a higher level of CD26 expression more likely to be linked to better response to chemotherapy. Moreover, CD26 expression was a significant factor associated with improved survival in patients who received chemotherapy [median survival time (MST), 18.6 vs. 10.7 months, P = 0.0083]. Furthermore, CD26 expression was significantly associated with better prognosis in patients receiving non-pemetrexed-containing regimens (MST, 14.2 vs. 7.4 months, P = 0.0042), whereas there was no significant association between CD26 expression and survival time for patients receiving pemetrexed-containing regimens. Our in vitro and microarray studies showed that mesothelioma cells expressing high CD26 displayed high proliferative activity, and CD26 expression was closely linked to cell-cycle regulation, apoptosis, and chemotherapy resistance.
  
  
  CONCLUSIONS
  Our results strongly suggest that CD26 is a clinically significant biomarker for predicting response to chemotherapy for MPM.
authors.affiliation: Department of Medical Oncology and Clinical Research, National Hospital Organization Yamaguchi-Ube Medical Center, Ube, Yamaguchi, Japan.
authors.forename: Keisuke
authors.initials: K
authors.lastname: Aoe
authors.forename: Vishwa Jeet
authors.initials: VJ
authors.lastname: Amatya
authors.forename: Nobukazu
authors.initials: N
authors.lastname: Fujimoto
authors.forename: Kei
authors.initials: K
authors.lastname: Ohnuma
authors.forename: Osamu
authors.initials: O
authors.lastname: Hosono
authors.forename: Akio
authors.initials: A
authors.lastname: Hiraki
authors.forename: Masanori
authors.initials: M
authors.lastname: Fujii
authors.forename: Taketo
authors.initials: T
authors.lastname: Yamada
authors.forename: Nam H
authors.initials: NH
authors.lastname: Dang
authors.forename: Yukio
authors.initials: Y
authors.lastname: Takeshima
authors.forename: Kouki
authors.initials: K
authors.lastname: Inai
authors.forename: Takumi
authors.initials: T
authors.lastname: Kishimoto
authors.forename: Chikao
authors.initials: C
authors.lastname: Morimoto
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D018819:Dipeptidyl Peptidase 4 / Q000235:genetics* / Q000378:metabolism; D005260:Female; D015870:Gene Expression; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic; D020868:Gene Silencing; D006801:Humans; D008297:Male; D008654:Mesothelioma / Q000188:drug therapy / Q000235:genetics* / Q000401:mortality*; D008875:Middle Aged; D010997:Pleural Neoplasms / Q000188:drug therapy / Q000235:genetics* / Q000401:mortality*; D016019:Survival Analysis; D016896:Treatment Outcome
chemical_list: D018819:Dipeptidyl Peptidase 4