Adenocarcinoma of the lung pathophysiology: Difference between revisions
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** [[Tyrosine kinase|Tyrosine kinase fusions]] | ** [[Tyrosine kinase|Tyrosine kinase fusions]] | ||
** ALK (2p23), ROS1 (6q22), and [[RET proto-oncogene|RET]] (10q11) | ** ALK (2p23), ROS1 (6q22), and [[RET proto-oncogene|RET]] (10q11) | ||
==Gross Pathology== | ==Gross Pathology== | ||
* On gross pathology, peripheral multifocal lesions are characteristic findings in patients with adenocarcinoma of the lung.<ref>Adenocarcinoma of the lung. Librepathology 2015. http://librepathology.org/wiki/index.php/File:Adenocarcinoma_%283950819000%29.jpg </ref> | * On gross pathology, peripheral multifocal lesions are characteristic findings in patients with adenocarcinoma of the lung.<ref>Adenocarcinoma of the lung. Librepathology 2015. http://librepathology.org/wiki/index.php/File:Adenocarcinoma_%283950819000%29.jpg </ref> | ||
Revision as of 18:04, 2 March 2018
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Adenocarcinoma of the Lung Microchapters |
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Differentiating Adenocarcinoma of the Lung from other Diseases |
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Diagnosis |
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Treatment |
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Case Studies |
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Adenocarcinoma of the lung pathophysiology On the Web |
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American Roentgen Ray Society Images of Adenocarcinoma of the lung pathophysiology |
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Risk calculators and risk factors for Adenocarcinoma of the lung pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Shanshan Cen, M.D. [2]
Overview
Genes involved in the pathogenesis of adenocarcinoma of the lung include EGFR, HER2, KRAS, ALK, and BRAF.[1] 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.
Pathogenesis
- Adenocarcinoma is the most common type of lung cancer found in non-smokers and is usually seen as a peripheral lesion in the lungs, as compared to centrally located tumors such as small cell lung cancer and squamous cell lung cancer.[2][3]
- Individual susceptibility, active smoking, radon exposure, exposure to high pollution levels, asbestos exposure, occupational or environmental exposure to particular agents or carcinogens contribute to the development of adenocarcinoma of the lung. Hydrocarbons cause damage to the DNA and form DNA adducts. Benzo-A-pyrine has effects on inducing p53 mutations and affects molecular signaling pathways such as AKT.
- The “multiple hit theory” for adenocarcinoma of the lung states that genetic reproduction is hindered due to the cumulative effect of several toxic insults. Underlying lung disease such as COPD, idiopathic pulmonary fibrosis and tuberculosis may exacerbate also trigger the process.
- Mutations involving several oncogenes may lead to the development of adenocarcinoma of the lung. These are as follows:
- Mutations of ras (found in thirty percent of cases) affect signal transduction by affecting GTPase activity:
- c-myc
- c-raf
- Tumor suppressor genes retinoblastoma (Rb) and p53
- Mutations of APOBEC protein
Genetics
Gross Pathology
- On gross pathology, peripheral multifocal lesions are characteristic findings in patients with adenocarcinoma of the lung.[7]
Microscopic Pathology
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
- Atypical adenomatous hyperplasia (AAH): is the precursor of peripheral adenocarcinomas. It consists of well demarcated columnar or cuboidal cells with the following features:[8][9]
- Varying degrees of cytologic atypia
- Hyperchromasia
- Pleomorphism
- Prominent nucleoli
- Nuclear atypia
- Eccentrically placed nuclei
- Abundant cytoplasm
- Conspicuous nucleoli
- Nuclear pseudoinclusions
- Lack of intercellular bridges
- On microscopic histopathological analysis, nuclear atypia, eccentrically placed nuclei, abundant cytoplasm, and conspicuous nucleoli are characteristic findings of adenocarcinoma of the lung.
- As adenocarcinoma is a derivative of mucus producing glands in the lungs, it tends to stain mucin positive.
- Based on differentiation, the tumor may be:
- Well differentiated (low grade) : normal appearance
- Poorly differentiated (high grade): abnormal glandular appearance with a positive mucin stain
Subtypes[10]
- Lepidic predominant
- Tumor grows long the alveolar wall
- Acinar predominant
- Berry-shaped glands, smaller than lung acini
- Papillary predominant
- Fibrovascular cores
- Micropapillary predominant
- Nipple shaped projections without fibrovascular cores
- Solid predominant
- Sheet of cells
Gross pathology
Gallery
-
![his subpleural lesion consists mostly of pigmented scar tissue with gray-tan tumor seen predominantly at the periphery.The visceral pleura overlying the tumor is retracted due to traction by underlying scar tissue. This is a good example of what has been called "scar carcinoma". In almost all cases of this type the scar is not a pre-existing lesion but rather represents a desmoplastic reponse to the tumor cells. The basal visceral pleura is involved by tumor[11]](/images/9/97/Lung_adenocarcinoma1.jpg)
his subpleural lesion consists mostly of pigmented scar tissue with gray-tan tumor seen predominantly at the periphery.The visceral pleura overlying the tumor is retracted due to traction by underlying scar tissue. This is a good example of what has been called "scar carcinoma". In almost all cases of this type the scar is not a pre-existing lesion but rather represents a desmoplastic reponse to the tumor cells. The basal visceral pleura is involved by tumor[11]
![his subpleural lesion consists mostly of pigmented scar tissue with gray-tan tumor seen predominantly at the periphery.The visceral pleura overlying the tumor is retracted due to traction by underlying scar tissue. This is a good example of what has been called "scar carcinoma". In almost all cases of this type the scar is not a pre-existing lesion but rather represents a desmoplastic reponse to the tumor cells. The basal visceral pleura is involved by tumor[11]](/index.php/File:Lung_adenocarcinoma1.jpg)
Microscopic Pathology
Gallery
-
![Micrograph of mucinous adenocarcinoma of the lung. H&E stain. [12]](/images/1/13/Lung_adenocarcinoma2.jpg)
Micrograph of mucinous adenocarcinoma of the lung. H&E stain. [12]
-
![Micrograph showing an adenocarcinoma of the lung (acinar pattern). H&E stain. [13]](/images/0/03/Lung_adenocarcinoma3.jpg)
Micrograph showing an adenocarcinoma of the lung (acinar pattern). H&E stain. [13]
![Micrograph of mucinous adenocarcinoma of the lung. H&E stain. [12]](/index.php/File:Lung_adenocarcinoma2.jpg)
![Micrograph showing an adenocarcinoma of the lung (acinar pattern). H&E stain. [13]](/index.php/File:Lung_adenocarcinoma3.jpg)
References
- ↑ Stewart, Bernard (2014). World cancer report 2014. Lyon, France Geneva, Switzerland: International Agency for Research on Cancer,Distributed by WHO Press, World Health Organization. ISBN 9283204298.
- ↑ Travis WD, Travis LB, Devesa SS (January 1995). "Lung cancer". Cancer. 75 (1 Suppl): 191–202. doi:10.1002/1097-0142(19950101)75:1+<191::AID-CNCR2820751307>3.0.CO;2-Y. PMID 8000996.
- ↑ Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson. "Chapter 13, box on morphology of adenocarcinoma". Robbins Basic Pathology (8th ed.). Philadelphia: Saunders. ISBN 1-4160-2973-7.
- ↑ Stewart, Bernard (2014). World cancer report 2014. Lyon, France Geneva, Switzerland: International Agency for Research on Cancer,Distributed by WHO Press, World Health Organization. ISBN 9283204298.
- ↑ Soda M, Choi YL, Enomoto M, Takada S, Yamashita Y, Ishikawa S; et al. (2007). "Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer". Nature. 448 (7153): 561–6. doi:10.1038/nature05945. PMID 17625570.
- ↑ Davies KD, Le AT, Theodoro MF, Skokan MC, Aisner DL, Berge EM; et al. (2012). "Identifying and targeting ROS1 gene fusions in non-small cell lung cancer". Clin Cancer Res. 18 (17): 4570–9. doi:10.1158/1078-0432.CCR-12-0550. PMC 3703205. PMID 22919003.
- ↑ Adenocarcinoma of the lung. Librepathology 2015. http://librepathology.org/wiki/index.php/File:Adenocarcinoma_%283950819000%29.jpg
- ↑ Kumar, Vinay (2007). Robbins basic pathology. Philadelphia, PA: Saunders/Elsevier. ISBN 1416029737.
- ↑ Stewart, Bernard (2014). World cancer report 2014. Lyon, France Geneva, Switzerland: International Agency for Research on Cancer,Distributed by WHO Press, World Health Organization. ISBN 9283204298.
- ↑ Adenocarcinoma of the lung. Librepathology 2015. http://librepathology.org/wiki/index.php/Adenocarcinoma_of_the_lung#Microscopic Accessed on December 20, 2015
- ↑ Adenocarcinoma of the lung. Librepathology 2015. http://librepathology.org/wiki/index.php/File:Adenocarcinoma_%283950819000%29.jpg
- ↑ Acinar adenocarcinoma. Librepathology 2015. http://librepathology.org/wiki/index.php/File:Mucinous_adenocarcinoma_of_the_lung_--_high_mag.jpg
- ↑ Mucinous adenocarcinoma. Librepathology 2015. http://librepathology.org/wiki/index.php/File:Acinar_pattern_adenocarcinoma_of_lung_--_intermed_mag.jpg
