Adenocarcinoma of the lung pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Shanshan Cen, M.D. [2] Sudarshana Datta, MD [3]

Overview

Adenocarcinoma is the most common type of lung cancer found in non-smokers and is usually seen as a peripheral lesion in the lungs. 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. Genes involved in the pathogenesis of adenocarcinoma of the lung include EGFR, HER2, KRAS, ALK, and BRAF. On gross pathology, peripheral multifocal lesions are characteristic findings in patients with adenocarcinoma of the lung. On microscopic histopathological analysis, nuclear atypia, eccentrically placed nuclei, abundant cytoplasm, and conspicuous nucleoli are characteristic findings of adenocarcinoma of the lung.

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.[1][2]

Genetics

Gross Pathology

  • On gross pathology, peripheral multifocal lesions are characteristic findings in patients with adenocarcinoma of the lung.[7]
Gray-tan tumor seen predominantly at the periphery.
Source: Libre pathology

Microscopic Pathology

Micrograph of mucinous adenocarcinoma of the lung, H&E stain.
Source: Libre pathology
Micrograph showing an adenocarcinoma of the lung (acinar pattern), H&E stain.
Source: Libre pathology



  • On microscopic histopathological analysis, nuclear atypia, eccentrically placed nuclei, abundant cytoplasm, and conspicuous nucleoli are characteristic findings of adenocarcinoma of the lung.
  • 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]
  • 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

  • Histologically adenocarcinoma is divided in to following subtypes:[10][11]
    • Lepidic adenocarcinoma[12][13]
      • Lepidic growth adenocarcinoma is defined as tumor cells proliferating along the surface of intact alveolar walls without stromal or vascular invasion pathologically.
    • Acinar adenocarcinoma
    • Papillary adenocarcinoma
    • Micropapillary adenocarcinoma
    • Solid adenocarcinoma
    • Invasive mucinous adenocarcinoma
      • Mixed invasive mucinous
      • Nonmucinous adenocarcinoma
    • Colloid adenocarcinoma
    • Fetal adenocarcinoma
    • Enteric adenocarcinoma
    • Minimally invasive adenocarcinoma
    • Nonmucinous
      • Mucinous
    • Preinvasive lesions
      • Atypical adenomatous hyperplasia
      • Adenocarcinoma in situ
        • Nonmucinous
        • Mucinous

References

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. 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.
  6. 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.
  7. Adenocarcinoma of the lung. Librepathology 2015. http://librepathology.org/wiki/index.php/File:Adenocarcinoma_%283950819000%29.jpg
  8. Kumar, Vinay (2007). Robbins basic pathology. Philadelphia, PA: Saunders/Elsevier. ISBN 1416029737.
  9. 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.
  10. Travis, William (2004). Pathology and genetics of tumours of the lung, pleura, thymus, and heart. Lyon: IARC Press. ISBN 9283224183.
  11. "www.jto.org".
  12. Iwata H (September 2016). "Adenocarcinoma containing lepidic growth". J Thorac Dis. 8 (9): E1050–E1052. doi:10.21037/jtd.2016.08.78. PMID 27747060.
  13. Jones KD (December 2013). "Whence lepidic?: the history of a Canadian neologism". Arch. Pathol. Lab. Med. 137 (12): 1822–4. doi:10.5858/arpa.2013-0144-HP. PMID 23937575.


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