title: Mitochondrial transcription factor a worsens the clinical course of patients with pancreatic cancer through inhibition of apoptosis of cancer cells.
abstract: OBJECTIVE
  Mitochondrial transcription factor A (mtTFA) is mandatory for both the transcription and maintenance of mitochondrial DNA. This study aimed to investigate the significance of mtTFA expression in pancreatic ductal adenocarcinoma (PDAC).
  
  
  METHODS
  Surgical specimens from 93 patients with PDAC who all underwent pancreatectomy were immunohistochemically stained using a polyclonal anti-mtTFA antibody. The relationship between the expression of mtTFA, clinicopathologic factors, and prognosis of these patients were evaluated.
  
  
  RESULTS
  Positive mtTFA expression was significantly associated with lymphovascular invasion and metastatic recurrence in the liver and correlated with an advanced surgical stage. A univariate analysis showed that the patients with positive mtTFA expression had a significantly shorter survival time than those patients with negative mtTFA expression, and a multivariate analysis revealed that mtTFA expression was one of the independent prognostic factors in patients with PDAC. Positive mtTFA expression was significantly correlated with a low apoptotic index but not significantly correlated with the mind bomb homolog-1 (MIB-1) index.
  
  
  CONCLUSIONS
  The expression mtTFA worsens the clinical course of patients with PDAC through the inhibition of apoptosis of PDAC cells and is an independent marker for the poor prognosis of the patients with PDAC after pancreatectomy. Mitochondrial transcription factor A may be a novel target for the treatment of PDAC.
authors.affiliation: From the *Department of Surgery 1, School of Medicine, University of Occupational and Environmental Health, Yahata-nishi-ku; and †Department of Gastroenterological and General Surgery, Wakamatsu Hospital of University of Occupational and Environmental Health, Wakamatsu-ku, Kitakyushu, Japan.
authors.forename: Masumi
authors.initials: M
authors.lastname: Yamauchi
authors.forename: Yoshifumi
authors.initials: Y
authors.lastname: Nakayama
authors.forename: Noritaka
authors.initials: N
authors.lastname: Minagawa
authors.forename: Takayuki
authors.initials: T
authors.lastname: Torigoe
authors.forename: Kazunori
authors.initials: K
authors.lastname: Shibao
authors.forename: Koji
authors.initials: K
authors.lastname: Yamaguchi
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D000368:Aged; D017209:Apoptosis; D021441:Carcinoma, Pancreatic Ductal / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D004277:DNA, Single-Stranded / Q000096:biosynthesis; D004268:DNA-Binding Proteins / Q000096:biosynthesis*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D053208:Kaplan-Meier Estimate; D019394:Ki-67 Antigen / Q000096:biosynthesis; D008297:Male; D008875:Middle Aged; D024101:Mitochondrial Proteins / Q000096:biosynthesis*; D015999:Multivariate Analysis; D010190:Pancreatic Neoplasms / Q000378:metabolism* / Q000473:pathology / Q000601:surgery; D011379:Prognosis; D014157:Transcription Factors / Q000096:biosynthesis*; D016896:Treatment Outcome
chemical_list: D004277:DNA, Single-Stranded; D004268:DNA-Binding Proteins; D019394:Ki-67 Antigen; D024101:Mitochondrial Proteins; D014157:Transcription Factors; C422562:mitochondrial transcription factor A