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| __NOTOC__ | | __NOTOC__ |
| {{Linitis plastica}} | | {{Linitis plastica}} |
| {{CMG}}{{AE}} {{STM}} | | {{CMG}};{{AE}}{{HM}} |
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| ==Overview== | | ==Overview== |
| On gross pathology, a thick, rigid, and leather bottle-like stomach wall is a characteristic finding of linitis plastica.<ref name=lp>Linitis plastica. Wikipedia. https://en.wikipedia.org/wiki/Linitis_plastica Accessed on November 18, 2015.</ref> On microscopic histopathological analysis, atypical [[signet ring cell]]s that diffusely infiltrate the stomach wall, [[submucosal]] [[fibrosis]] and thickening, and a minimal [[mucosa]]l involvement are characteristic findings of linitis plastica. Development of linitis plastica is the result of genetic mutation in the ''CDH1'' ([[E-cadherin]]) gene, that is responsible for intercellular adhesions.<ref name name=mk>Gastric linitis plastica. Orphanet. http://www.orpha.net/consor/cgi-bin/OC_Exp.php?Lng=GB&Expert=36273 Accessed on December 8, 2015.</ref>
| | The exact pathogenesis of [disease name] is not fully understood. |
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| ==Pathogenesis==
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| *Linitis plastica is a morphological variant of diffuse (or infiltrating) gastric adenocarcinoma.<ref name=lp>Linitis plastica. Wikipedia. https://en.wikipedia.org/wiki/Linitis_plastica Accessed on November 12, 2015.</ref>
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| * Linitis plastica may also occur secondary to metastasis from other primary cancers, particularly infiltrating lobular carcinoma of breast. | | 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]. |
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| | [Pathogen name] is usually transmitted via the [transmission route] route to the human host. |
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| | Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell. |
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| | Linitis plastica arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells]. |
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| | The progression to [disease name] usually involves the [molecular pathway]. |
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| | The pathophysiology of [disease/malignancy] depends on the histological subtype. |
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| | ==Pathophysiology== |
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| | ===Pathogenesis=== |
| | *The exact pathogenesis of [disease name] is not fully understood. |
| | OR |
| | *It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3]. |
| | *[Pathogen name] is usually transmitted via the [transmission route] route to the human host. |
| | *Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell. |
| | *[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells]. |
| | *The progression to [disease name] usually involves the [molecular pathway]. |
| | *The pathophysiology of [disease/malignancy] depends on the histological subtype. |
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| ==Genetics== | | ==Genetics== |
| *[[Germline]] mutations in the ''CDH1'' ([[E-cadherin]]) gene, which results in an altered intercellular adhesions, may be involved in the pathogenesis of diffuse gastric adenocarcinoma.<ref name=mk>Gastric linitis plastica. Orphanet. http://www.orpha.net/consor/cgi-bin/OC_Exp.php?Lng=GB&Expert=36273 Accessed on November 19, 2015.</ref><ref name="WolfGeigl2010">{{cite journal|last1=Wolf|first1=E.-M.|last2=Geigl|first2=J.B.|last3=Svrcek|first3=M.|last4=Vieth|first4=M.|last5=Langner|first5=C.|title=Hereditäres Magenkarzinom|journal=Der Pathologe|volume=31|issue=6|year=2010|pages=423–429|issn=0172-8113|doi=10.1007/s00292-010-1353-7}}</ref> | | *[Disease name] is transmitted in [mode of genetic transmission] pattern. |
| *Hereditary form of diffuse gastric adenocarcinoma is transmitted in an [[autosomal dominant]] fashion, with a 70% disease [[penetrance]].<ref name=mk>Gastric linitis plastica. Orphanet. http://www.orpha.net/consor/cgi-bin/OC_Exp.php?Lng=GB&Expert=36273 Accessed on November 19, 2015.</ref><ref name="WolfGeigl2010">{{cite journal|last1=Wolf|first1=E.-M.|last2=Geigl|first2=J.B.|last3=Svrcek|first3=M.|last4=Vieth|first4=M.|last5=Langner|first5=C.|title=Hereditäres Magenkarzinom|journal=Der Pathologe|volume=31|issue=6|year=2010|pages=423–429|issn=0172-8113|doi=10.1007/s00292-010-1353-7}}</ref> | | *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. |
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| | ==Associated Conditions== |
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| ==Gross Pathology== | | ==Gross Pathology== |
| *On gross pathology, thick, rigid, leather bottle-like stomach from diffuse infiltration of the stomach wall is a characteristic finding of linitis plastica.<ref name=lp>Linitis plastica. Wikipedia. https://en.wikipedia.org/wiki/Linitis_plastica Accessed on November 18, 2015.</ref> | | *On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name]. |
| *[[Metastasis]] to the [[peritoneum]], [[lymph node]]s, and/or other organs usually occurs by the time linitis plastica is diagnosed.<ref name=mk>Gastric linitis plastica. Orphanet. http://www.orpha.net/consor/cgi-bin/OC_Exp.php?Lng=GB&Expert=36273 Accessed on December 7, 2015.</ref>
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| <gallery>
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| image:Linitis_plastica1.jpg|Endoscopic image of linitis plastica, a type of stomach cancer where the entire stomach is invaded, leading to a leather bottle-like appearance with blood coming out of it.<ref>Linitis Plastica. Wikimedia. https://en.wikipedia.org/wiki/Linitis_plastica#/media/File:Linitis_plastica_2.jpg Accessed on December 13, 2015</ref></gallery>
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| ==Microscopic Pathology== | | ==Microscopic Pathology== |
| *In diffuse type adenocarcinoma (mucinous, [[colloid]]), tumour cells are discohesive and secrete mucus, which is delivered in the [[interstitium]], producing large pools of mucus or colloid (optically "empty" spaces). If the mucus remains inside the tumour cell, it pushes the nucleus to the periphery, leaving a "signet-ring cell" appearance.
| | *On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name]. |
| *On microscopic histopathological analysis, atypical [[signet ring cell]]s that diffusely infiltrate the stomach wall, [[submucosal]] [[fibrosis]] and thickening, and a minimal [[mucosa]]l involvement are characteristic findings of linitis plastica.<ref name="SchauerPeiper2011">{{cite journal|last1=Schauer|first1=M|last2=Peiper|first2=M|last3=Theisen|first3=J|last4=Knoefel|first4=W|title=Prognostic factors in patients with diffuse type gastric cancer (linitis plastica) after operative treatment|journal=European Journal of Medical Research|volume=16|issue=1|year=2011|pages=29|issn=2047-783X|doi=10.1186/2047-783X-16-1-29}}</ref><ref>Stomach cancer. Wikipedia. https://en.wikipedia.org/wiki/Stomach_cancer Accessed on November 19, 2015.</ref> | |
| *Superficial mucosal layers are usually spared and rarely show superficial ulcers on endoscopy, that has a wide differential diagnosis, making the diagnosis even more difficult. The biopsies are falsely negative, as the disease remains mostly in the [[submucosa]] and muscularis propria.<ref name="SchauerPeiper2011">{{cite journal|last1=Schauer|first1=M|last2=Peiper|first2=M|last3=Theisen|first3=J|last4=Knoefel|first4=W|title=Prognostic factors in patients with diffuse type gastric cancer (linitis plastica) after operative treatment|journal=European Journal of Medical Research|volume=16|issue=1|year=2011|pages=29|issn=2047-783X|doi=10.1186/2047-783X-16-1-29}}</ref>
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| *Although the lower [[mucosa]]l and [[submucosa]]l layers are mostly involved, the muscular and subserosal layers may also be infiltrated with the neoplastic cells.<ref>{{Cite journal
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| | author = [[Bing Hu]], [[Nassim El Hajj]], [[Scott Sittler]], [[Nancy Lammert]], [[Robert Barnes]] & [[Aurelia Meloni-Ehrig]]
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| | title = Gastric cancer: Classification, histology and application of molecular pathology
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| | journal = [[Journal of gastrointestinal oncology]]
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| | volume = 3
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| | issue = 3
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| | pages = 251–261
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| | year = 2012
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| | month = September
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| | doi = 10.3978/j.issn.2078-6891.2012.021
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| | pmid = 22943016
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| }}</ref>
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| ==Gallery==
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| <gallery>
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| image:Gastric_signet_ring_cell_carcinoma.jpg|A signet ring cell carcinoma of the stomach. Signet ring cells are seen in the lower half of the image. Gastric epithelium is seen in the upper half of the image. H&E stain.<ref>Linitis Plastica. Wikimedia. https://en.wikipedia.org/wiki/Signet_ring_cell_carcinoma#/media/File:Signet_ring_cell_carcinoma_-_very_high_mag.jpg Accessed on December 13, 2015</ref>
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| image:Gastric_signet_ring_cell_carcinomahistopatholgy.jpg|Gastric signet ring cell carcinoma. H&E stain.<ref>Linitis Plastica. Wikimedia.https://en.wikipedia.org/wiki/Signet_ring_cell_carcinoma#/media/File:Gastric_signet_ring_cell_carcinoma_histopatholgy_%281%29.jpg Accessed on December 13, 2015.</ref>
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| </gallery>
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| ==References== | | ==References== |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Hadeel Maksoud 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
Linitis plastica 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 exact pathogenesis of [disease name] is not fully understood.
OR
- It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
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
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