title: Expression of CAS/CSE1L, the Cellular Apoptosis Susceptibility Protein, Correlates With Neoplastic Progression in Barrett's Esophagus.
abstract: Identifying the molecular switch responsible for the neoplastic progression of Barrett's esophagus (BE) and initiation of adenocarcinoma (ADC) is clinically essential and it will have a profound impact on patient diagnosis, prognosis, and treatment. The cellular apoptosis susceptibility gene CAS/CSE1L is overexpressed in various cancers, including a rare report on esophageal ADC; however, its expression in BE neoplasia has not been addressed.
  
  
  
  We investigated the expression of the CAS/CSE1L protein immunohistochemically in 56 esophageal resection specimens for ADC arising in BE. For each specimen, a full representative section of the invasive ADC was selected to include, when possible, BE, low-grade dysplasia (LGD) and high-grade dysplasia (HGD). Samples were stained for CAS/CSE1L expression using a rabbit polyclonal antibody recognizing the N-terminus of human CAS/CSE1L. Protein expression levels were measured using the Allred semiquantitative scoring system. The data were evaluated using χ statistical analysis. Gene expression Omnibus was queried for CAS/CSE1L and BE neoplasia.
  
  
  
  We found minimal to absent CAS/CSE1L in all BE tissue samples; however, CAS/CSE1L was upregulated in 60% of LGD and overexpressed in HGD and ADC. The results were statistically significant (P<0.05). The localization of CAS/CSE1L protein was nuclear in BE; it became nuclear and cytoplasmic in LGD and HGD, and predominantly cytoplasmic in ADC. A similar progressive increase was observed for CAS/CSE1L gene expression.
  
  
  
  These findings show changes in CAS/CSE1L during BE progression. CAS/CSE1L may represent a potential marker for dysplasia/carcinoma.
authors.affiliation: Departments of Anatomic Pathology.|Oncological Sciences, University of South Florida, Tampa, FL.
authors.forename: Kun
authors.initials: K
authors.lastname: Jiang
authors.affiliation: Departments of Anatomic Pathology.
authors.forename: Kevin
authors.initials: K
authors.lastname: Neill
authors.affiliation: Departments of Anatomic Pathology.
authors.forename: Daniel
authors.initials: D
authors.lastname: Cowden
authors.affiliation: Oncological Sciences, University of South Florida, Tampa, FL.|Gastrointestinal Oncology.
authors.forename: Jason
authors.initials: J
authors.lastname: Klapman
authors.affiliation: Oncological Sciences, University of South Florida, Tampa, FL.|Bioinformatics, H. Lee Moffitt Cancer Center and Research Institute.
authors.forename: Steven
authors.initials: S
authors.lastname: Eschrich
authors.affiliation: Oncological Sciences, University of South Florida, Tampa, FL.|Gastrointestinal Oncology.
authors.forename: José
authors.initials: J
authors.lastname: Pimiento
authors.affiliation: Oncological Sciences, University of South Florida, Tampa, FL.|Gastrointestinal Oncology.
authors.forename: Mokenge P
authors.initials: MP
authors.lastname: Malafa
authors.affiliation: Departments of Pathology and Cell Biology.|Chemical Biology Molecular and Medicine.|Tumor Biology.
authors.forename: Domenico
authors.initials: D
authors.lastname: Coppola
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism* / Q000473:pathology; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001471:Barrett Esophagus / Q000378:metabolism* / Q000473:pathology; D014408:Biomarkers, Tumor / Q000096:biosynthesis*; D029563:Cellular Apoptosis Susceptibility Protein / Q000096:biosynthesis*; D004938:Esophageal Neoplasms / Q000378:metabolism* / Q000473:pathology; D004947:Esophagus / Q000378:metabolism* / Q000473:pathology; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D006965:Hyperplasia / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000096:biosynthesis*
chemical_list: D014408:Biomarkers, Tumor; D029563:Cellular Apoptosis Susceptibility Protein; D009363:Neoplasm Proteins