CC BY-NC-ND 4.0 · Indian J Med Paediatr Oncol 2017; 38(03): 326-327
DOI: 10.4103/ijmpo.ijmpo_111_17
Original Article

Physiogenomics in Etiopathogenesis of Cholangiocarcinoma

Beuy Joob
Sanitation 1 Medical Academic Center, Bangkok, Thailand
,
Viroj Wiwanitkit
Department of Tropical Medicine, Hainan Medical University, Haikou, China
› Author Affiliations
Financial support and sponsorship Nil.

Abstract

Objective: Cholangiocarcinoma is a serious malignancy that is very common in the tropical countries. It is a kind of deadly primary hepatobiliary tumor. There is a wide spectrum of tumors with varying differentiation and malignancy grades. Although it has been known for a long time inmmedicine, there is no clear cut that this deadly cancer is genetic disorder or not. A systemic approach on the pathophysiology and genomics can provide useful information and help better understand the pathogenesis of cholangiocarcinoma. Methods: In this work, a standard bioinformatics physiological genomics analysis of cholangiocarcinoma was performed. Result: According to this work, there is no identified physiogenomics relationship for the cholangiocarcinoma. Conclusion: This might imply that the cholangiocarcinoma is directly due to environmental insult. It implies that there should be no specific gene that might contribute to the increased risk in the etiopathogenesis of cholangiocarcinoma.



Publication History

Article published online:
04 July 2021

© 2017. Indian Society of Medical and Paediatric Oncology. This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial-License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/.)

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  • References

  • 1 Schlesinger LB. Physiognomic perception: Empirical and theoretical perspectives. Genet Psychol Monogr 1980;101:71-97.
  • 2 Khan SA, Thomas HC, Davidson BR, Taylor-Robinson SD. Cholangiocarcinoma. Lancet 2005;366:1303-14.
  • 3 Patel T. Cholangiocarcinoma. Nat Clin Pract Gastroenterol Hepatol 2006;3:33-42.
  • 4 Ghirardello S, Malattia C, Scagnelli P, Maghnie M. Current perspective on the pathogenesis of central diabetes insipidus. J Pediatr Endocrinol Metab 2005;18:631-45.
  • 5 Isezuo SA. The metabolic syndrome: Review of current concepts. Niger Postgrad Med J 2006;13:247-55.
  • 6 Cowley AW Jr., Roman RJ, Jacob HJ. Application of chromosomal substitution techniques in gene-function discovery. J Physiol 2004;554:46-55.
  • 7 Cowley AW Jr., Liang M, Roman RJ, Greene AS, Jacob HJ. Consomic rat model systems for physiological genomics. Acta Physiol Scand 2004;181:585-92.
  • 8 Wiwanitkit V. Physiological genomics analysis for mania: Supportive evidence for epigenetics concept. Indian J Psychol Med 2014;36:366-7.
  • 9 Wiwanitkit S, Wiwanitkit V. Relationship between schizophrenia and diabetes mellitus: Consideration based on physiogenomics data. Indian J Psychol Med 2013;35:223-4.
  • 10 Wiwanitkit V. Physiological genomics analysis for Alzheimer's disease. Ann Indian Acad Neurol 2013;16:72-4.
  • 11 Wiwanitkit V. Physiological genomics analysis for central diabetes insipidus. Acta Neurol Taiwan 2008;17:214-6.
  • 12 Wiwanitkit V. Difference in physiogenomics between male and female infertility. Andrologia 2008;40:158-60.
  • 13 Alison MR. Liver cancer: A disease of stem cells? Panminerva Med 2006;48:165-74.
  • 14 Alison MR. Liver stem cells: Implications for hepatocarcinogenesis. Stem Cell Rev 2005;1:253-60.
  • 15 Miller CR, Perry A. Glioblastoma. Arch Pathol Lab Med 2007;131:397-406.
  • 16 Sandhu DS, Shire AM, Roberts LR. Epigenetic DNA hypermethylation in cholangiocarcinoma: Potential roles in pathogenesis, diagnosis and identification of treatment targets. Liver Int 2008;28:12-27.
  • 17 Cheng W, Qi Y, Tian L, Wang B, Huang W, Chen Y, et al. Dicer promotes tumorigenesis by translocating to nucleus to promote SFRP1 promoter methylation in cholangiocarcinoma cells. Cell Death Dis 2017;8:e2628.