Pancreatic cancer pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
*The | *The pathogenesis of pancreatic cancer involves the activation or inactivation of multiple gene subsets and their interaction. | ||
*The molecular pathogenesis of pancreatic cancer involves the following: | |||
* | **Inactivation of tumor suppressor genes | ||
* | **Activation of oncogenes | ||
* | **Deregulation of molecules in various signalling pathways | ||
* | ***EGFR | ||
* | ***Akt | ||
* | ***NF-kB | ||
***Hedgehog pathways | |||
==Genetics== | ==Genetics== | ||
*[Disease name] is transmitted in [mode of genetic transmission] pattern. | *[Disease name] is transmitted in [mode of genetic transmission] pattern. |
Revision as of 15:25, 10 November 2017
https://https://www.youtube.com/watch?v=XFxMOiJRZQg%7C350}} |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Parminder Dhingra, M.D. [2]
Pancreatic cancer Microchapters |
Diagnosis |
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Treatment |
Case Studies |
Pancreatic cancer pathophysiology On the Web |
American Roentgen Ray Society Images of Pancreatic cancer pathophysiology |
Risk calculators and risk factors for Pancreatic cancer pathophysiology |
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 pathogenesis of pancreatic cancer involves the activation or inactivation of multiple gene subsets and their interaction.
- The molecular pathogenesis of pancreatic cancer involves the following:
- Inactivation of tumor suppressor genes
- Activation of oncogenes
- Deregulation of molecules in various signalling pathways
- EGFR
- Akt
- NF-kB
- Hedgehog pathways
Genetics
- [Disease name] is transmitted in [mode of genetic transmission] pattern.
- Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
- The development of [disease name] is the result of multiple genetic mutations.
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
Overview
The pathophysiology of pancreatic adenocarcinoma includes considerable desmoplasia or formation of a dense fibrous stroma or structural tissue consisting of a range of cell types (including myofibroblasts, macrophages, lymphocytes and mast cells) and deposited material (such as type I collagen and hyaluronic acid).
Pathophysiology
Pathology
The most common form of pancreatic cancer (adenocarcinoma) is typically characterized by moderately to poorly differentiated glandular structures on microscopic examination. There is typically considerable desmoplasia or formation of a dense fibrous stroma or structural tissue consisting of a range of cell types (including myofibroblasts, macrophages, lymphocytes and mast cells) and deposited material (such as type I collagen and hyaluronic acid).