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Published byIsabela Lencastre Valgueiro Modified over 5 years ago
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Duodenal Reflux Leads to Down Regulation of DNA Mismatch Repair Pathway in an Animal Model of Esophageal Cancer Pramod Bonde, MD, MS, Daqing Gao, PhD, Lei Chen, PhD, Tomoharu Miyashita, MD, Elizabeth Montgomery, MD, PhD, John W. Harmon, MD, Chiming Wei, MD, PhD The Annals of Thoracic Surgery Volume 83, Issue 2, Pages (February 2007) DOI: /j.athoracsur Copyright © 2007 The Society of Thoracic Surgeons Terms and Conditions
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Fig 1 (A) Representative histology section shows adenocarcinoma of the esophagus in the reflux induced rat model. (B) Histology section shows a squamous cell cancer of esophagus from the reflux group treated with methyl-n-amyl nitrosamine (MNAN). The Annals of Thoracic Surgery , DOI: ( /j.athoracsur ) Copyright © 2007 The Society of Thoracic Surgeons Terms and Conditions
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Fig 2 (A) Representative 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxoG) staining in normal, adenocarcinoma (ADC) and squamous cell cancer (SCC) of the esophagus. The positive staining for 8-oxoG was found in the nucleus of esophageal cancer cells in both ADC and SCC (arrows), but no positive staining of 8-oxoG was found in normal esophageal mucosal cells (original magnification ×1000). (B) Quantitative analysis of 8-oxoG staining indicates that the 8-oxoG level was significantly increased in ADC and SCC compared with normal esophagus. (Data shown are ± SE; p < 0.01 vs. normal). The Annals of Thoracic Surgery , DOI: ( /j.athoracsur ) Copyright © 2007 The Society of Thoracic Surgeons Terms and Conditions
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Fig 3 (A) A representative immunohistochemical staining with Mut Y homologue (MYH) antibody in normal rat esophagus, adenocarcinoma (ADC) and squamous cell cancer (SCC). The expression of MYH was localized in nuclear and perinuclear region. The staining density of human MYH was markedly decreased in both ADC and SCC compared with normal rat esophagus (original magnification ×1000). (B) Quantitative analysis of MYH staining demonstrates that positive MYH staining density was significantly decreased in reflux-induced ADC and reflux and carcinogen-treated SCC compared with normal rat esophagus. (Data shown are ± SE.) The Annals of Thoracic Surgery , DOI: ( /j.athoracsur ) Copyright © 2007 The Society of Thoracic Surgeons Terms and Conditions
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Fig 4 Representative Western blot analysis with MYH antibody in normal rat esophageal tissue, adenocarcinoma (ADC) tissue, and squamous cell cancer (SCC) tissue. Protein expression of MYH was markedly reduced in the ADC and SCC tissues. Western blot of actin was used to monitor equal loading. The Annals of Thoracic Surgery , DOI: ( /j.athoracsur ) Copyright © 2007 The Society of Thoracic Surgeons Terms and Conditions
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Fig 5 (A) Terminal deoxynucleotide transferase-mediated deoxy uridine triphosphate nick-end labeling (TUNEL) staining in normal rat esophagus, adenocarcinoma (ADC,) and squamous cell cancer (SCC). The positive TUNEL staining (arrows) was markedly increased in both ADC and SCC when compared to normal rat esophagus (original magnification ×1000) (B) Quantitative analysis of TUNEL staining demonstrates significant DNA fragmentation in the ADC and SCC groups compared with normal rat esophagus. (Data shown are ± SEM.) The Annals of Thoracic Surgery , DOI: ( /j.athoracsur ) Copyright © 2007 The Society of Thoracic Surgeons Terms and Conditions
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