Staging of biliary atresia at diagnosis by molecular profiling of the liver
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* Corresponding author: Jorge A Bezerra Jorge.bezerra@cchmc.org
1 Division of Pediatric Gastroenterology, Hepatology and Nutrition of Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229, USA
2 Division of Pediatric Pathology, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229, USA
3 Department of Environmental Health, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267, USA
4 Department of Surgery of the University of Michigan Medical School, 1500 E. Medical Center Drive, Ann Arbor, MI 48109, USA
5 Current address: Children's Pathology Services, Children's Hospitals and Clinics of Minnesota, 2525 Chicago Avenue, Minneapolis, MN 55404, USA
6 Division of Biomedical Informatics, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229, USA
Genome Medicine 2010, 2:33 doi:10.1186/gm154
Published: 13 May 2010Additional files
Additional file 1:
Data elements and rationale for inclusion in the study.
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Additional file 2:
Description of PCR primers.
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Additional file 3:
Description of subjects enrolled in the study.
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Additional file 4:
Genes that are up-regulated in subjects with hepatic inflammation or fibrosis.
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Additional file 5:
Transcription factors in subjects with hepatic inflammation or fibrosis.
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Additional file 6:
Genes containing transcription factor binding sites for NFκB or SP1.
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Additional file 7:
Figures of the relationship between histological groups with age and survival. (a) The probability density function of age at the time of surgery (Kasai procedure) in relation to histological scores ≥1 for inflammation or fibrosis in biliary atresia (P = 0.7). The age of individual patient is shown below the graph as short vertical bars. (b) Kaplan-Meier analysis shows similar survival with the native liver in infants belonging to either group (P = 0.48).
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