Cholangiocarcinoma pathophysiology: Difference between revisions
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==Genetics== | ==Genetics== | ||
Molecular mechanism of cholangiocarcinoma | <div style="text align: center>'''Molecular mechanism of cholangiocarcinoma'''</div> | ||
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Revision as of 20:08, 2 February 2018
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Risk calculators and risk factors for Cholangiocarcinoma pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]
Overview
The exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Pathogenesis
- The epithelial cell lining the bile ducts are called cholangiocytes. The malignant transformsation of cholangiocytes leads to cholangiocarcinoma.[1]
- Malignant transformation of cholangiocytes into cholangiocarcinoma include following stages:[2]
- Hyperplasia
- Metaplasia
- Dysplasia
- Frank carcinoma
- Progression of malignancy is believed to be due to:[2][3][4]
- Inflammation
- Obstruction of bile ducts
- Biliary intraepithelia neoplasia
- Biliary intraepithelial neoplasia is believed to be the initial lesion of cholangiocarcinoma, particularly in patients with hepatolithiasis in bile ducts.
Genetics
| Cholangiocytes | |||||||||||||||||||||||||||||||
| Proinflammatory cytokines (TNF-α and IL-6) | |||||||||||||||||||||||||||||||
| Several cytokines ) | Stimulates the expression of inducible nitric oxide synthase (iNOS) and enhancing NO production | Reactive oxygen species | |||||||||||||||||||||||||||||
| EGFR (epidermal growth factor receptor) family, specifically the tyrosine kinase ErbB-2 (HER2/neu | Inhibit DNA repair mechanism | ||||||||||||||||||||||||||||||
| Stimulation of cyclooxygenase 2 (COX-2) | Nitrosylation of caspase | ||||||||||||||||||||||||||||||
| Increased invasiveness, proliferation, and mobility of cholangiocytes | |||||||||||||||||||||||||||||||
| Prostaglandin E2 production(Rate limitimg step) | |||||||||||||||||||||||||||||||
| Activate cell cycle of cholangiocytes | Inhibit apoptosis of cholangiocytes | Promotes mutagenesis | |||||||||||||||||||||||||||||
Associated Conditions
Gross Pathology
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ Fava, G.; Lorenzini, I. (2012). "Molecular Pathogenesis of Cholangiocarcinoma". International Journal of Hepatology. 2012: 1–7. doi:10.1155/2012/630543. ISSN 2090-3448.
- ↑ 2.0 2.1 Sirica A (2005). "Cholangiocarcinoma: molecular targeting strategies for chemoprevention and therapy". Hepatology. 41 (1): 5–15. PMID 15690474.
- ↑ Holzinger F, Z'graggen K, Büchler M. "Mechanisms of biliary carcinogenesis: a pathogenetic multi-stage cascade towards cholangiocarcinoma". Ann Oncol. 10 Suppl 4: 122–6. PMID 10436802.
- ↑ Gores G (2003). "Cholangiocarcinoma: current concepts and insights". Hepatology. 37 (5): 961–9. PMID 12717374.