Accepted
at 12:35 a.m. Nov, 01, 2023
by
Joe
Author:
jewbacca
Type of change:
Updated content
Rationale for change
changed the cloze2 to include "microsatellite instability" instead of just "microsatellite". "Instability" gives the card away because we are primed to guess microsatellite before instability; this version better tests whether you can distinguish microsatellite instability vs adenoma-carcinoma pathways
Before
After
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Extra
e.g., MLH1, MSH2
Lecture Notes
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Missed Questions
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Pathoma
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Boards and Beyond
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First Aid
Sketchy
Watch Colorectal Polyps & Cancer
* (Lynch Syndrome)
Watch Colorectal Polyps & Cancer
Sketchy 2
Watch Colorectal Cancer: Carcinogenesis
Watch Colorectal Cancer: Carcinogenesis
Sketchy Extra
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Picmonic
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Pixorize
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Physeo
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Bootcamp
Watch associated Bootcamp video - Large Intestine : Colorectal Cancer
Watch associated Bootcamp video - Colorectal Pathology : Hereditary Polyposis
Watch associated Bootcamp video - Large Intestine : Colorectal Carcinogenesis Molecular Pathway
Watch associated Bootcamp video - Colorectal Pathology : Hereditary Polyposis
Watch associated Bootcamp video - Large Intestine : Colorectal Carcinogenesis Molecular Pathway
OME
Additional Resources
Atlas:
Colorectal carcinogenesis pathways
Top: Chromosomal instability pathway (adenoma-carcinoma sequence)
- Loss of the tumor suppressor gene, APC, results in hyperproliferative epithelium due to a loss of cellular adhesion and increased cellular proliferation. A mutation in KRAS results in unregulated cellular signaling and cellular proliferation, leading to the formation of an adenoma. Loss of the tumor suppressor genes TP53 and DCC results in the malignant transformation of an adenoma to carcinoma. The chromosomal instability pathway is responsible for carcinomas in FAP (loss of APC) as well as in most cases of sporadic colorectal carcinoma.
- Loss of the tumor suppressor gene, APC, results in hyperproliferative epithelium due to a loss of cellular adhesion and increased cellular proliferation. A mutation in KRAS results in unregulated cellular signaling and cellular proliferation, leading to the formation of an adenoma. Loss of the tumor suppressor genes TP53 and DCC results in the malignant transformation of an adenoma to carcinoma. The chromosomal instability pathway is responsible for carcinomas in FAP (loss of APC) as well as in most cases of sporadic colorectal carcinoma.
Bottom: Microsatellite instability pathway
- Acquired or inherited mutations in the mismatch repair genes (esp. MLH1 and MSH2) result in abnormal proliferation and the formation of adenoma and carcinoma. The microsatellite instability pathway is responsible for carcinomas in Lynch syndrome (HNPCC) and a few cases of sporadic colorectal carcinoma.
- Acquired or inherited mutations in the mismatch repair genes (esp. MLH1 and MSH2) result in abnormal proliferation and the formation of adenoma and carcinoma. The microsatellite instability pathway is responsible for carcinomas in Lynch syndrome (HNPCC) and a few cases of sporadic colorectal carcinoma.
Atlas:
One by one
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