Basal cell carcinoma pathophysiology: Difference between revisions
Created page with " {{Basal cell carcinoma}} {{CMG}} ==Overview== ==References== {{reflist|2}} {{Epithelial neoplasms}} {{Diseases of the skin and appendages by morphology}} {{Tumors of bone, ..." |
No edit summary |
||
| Line 1: | Line 1: | ||
{{Basal cell carcinoma}} | {{Basal cell carcinoma}} | ||
{{CMG}} | {{CMG}} | ||
== | |||
==Pathophysiology== | |||
[[Image:basal cell carcinoma pathology.jpg|left|thumb|200px|Histology of a nodular basal cell carcinoma]] | |||
Basal cell carcinomas develop in the [[basal cell layer]] of the [[skin]]. Sun light exposure leads to the formation of [[thymine dimer]]s, a form of DNA damage. | |||
While [[DNA repair]] removes most UV-induced damage, not all crosslinks are excised. There is, therefore, cumulative DNA damage leading to [[mutation]]s. Apart from the mutagenesis, sunlight depresses the local [[immune system]], possibly decreasing immune surveillance for new tumor cells. | |||
Basal-cell carcinoma also develops as a result of basal-cell nevus syndrome, or Gorlin's syndrome, which is also characterized by odontogenic keratocysts of the jaw, palmar or plantar (sole of the foot) pits, calcification of the [[falx cerebri]] (in the center line of the brain) and rib abnormalities. | |||
The cause of the syndrome is a mutation in the [[PTCH1]] tumor-suppressor gene at chromosome 9q22.3, which inhibits the [[hedgehog signaling pathway]]. A mutation in the [[smoothened|SMO]] gene, which is also on the hedgehog pathway, also causes basal-cell carcinoma.<ref>{{cite journal |author=Epstein EH, Shepard JA, Flotte TJ |title=Case records of the Massachusetts General Hospital. Case 3-2008. An 80-year-old woman with cutaneous basal-cell carcinomas and cysts of the jaws |journal=N Engl J Med |volume=358 |issue=4 |pages=393–401 |year=2008 |month=Jan |pmid=18216361 |doi=10.1056/NEJMcpc0707893 |url=}}</ref> | |||
==References== | ==References== | ||
Revision as of 18:33, 19 January 2012
|
Basal cell carcinoma Microchapters |
|
Diagnosis |
|---|
|
Case Studies |
|
Basal cell carcinoma pathophysiology On the Web |
|
American Roentgen Ray Society Images of Basal cell carcinoma pathophysiology |
|
Risk calculators and risk factors for Basal cell carcinoma pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
Basal cell carcinomas develop in the basal cell layer of the skin. Sun light exposure leads to the formation of thymine dimers, a form of DNA damage.
While DNA repair removes most UV-induced damage, not all crosslinks are excised. There is, therefore, cumulative DNA damage leading to mutations. Apart from the mutagenesis, sunlight depresses the local immune system, possibly decreasing immune surveillance for new tumor cells.
Basal-cell carcinoma also develops as a result of basal-cell nevus syndrome, or Gorlin's syndrome, which is also characterized by odontogenic keratocysts of the jaw, palmar or plantar (sole of the foot) pits, calcification of the falx cerebri (in the center line of the brain) and rib abnormalities.
The cause of the syndrome is a mutation in the PTCH1 tumor-suppressor gene at chromosome 9q22.3, which inhibits the hedgehog signaling pathway. A mutation in the SMO gene, which is also on the hedgehog pathway, also causes basal-cell carcinoma.[1]
References
- ↑ Epstein EH, Shepard JA, Flotte TJ (2008). "Case records of the Massachusetts General Hospital. Case 3-2008. An 80-year-old woman with cutaneous basal-cell carcinomas and cysts of the jaws". N Engl J Med. 358 (4): 393–401. doi:10.1056/NEJMcpc0707893. PMID 18216361. Unknown parameter
|month=ignored (help)
Template:Tumors of bone, cartilage, skin, connective, and soft tissue
Template:SIB
de:Basaliom
nl:Basaalcelcarcinoom
fi:Basaliooma