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Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
Published on: July 28, 2010
Sonic hedgehog relates to colorectal carcinogenesis.
Kozo Yoshikawa1, Mitsuo Shimada, Hidenori Miyamoto
1Department of Surgery, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Tokushima, Japan.
Journal of Gastroenterology
|August 8, 2009
Summary
Sonic hedgehog (Shh) signaling is activated in colorectal adenomas and progresses with tumor development. This suggests Shh may trigger the adenoma-carcinoma sequence, offering a potential therapeutic target for hedgehog blockade in cancer.
Area of Science:
- Gastrointestinal Oncology
- Molecular Biology
- Cancer Research
Background:
- Hedgehog signaling is crucial for gastrointestinal development.
- Aberrant Hedgehog signaling, particularly Sonic hedgehog (Shh), is linked to various cancers, including colorectal cancer.
- Pancreatic precursor lesions show elevated Shh expression compared to normal and cancerous tissues.
Purpose of the Study:
- To investigate Sonic hedgehog (Shh) related protein expression in colorectal hyperplastic polyps and the adenoma-carcinoma sequence.
- To compare Shh, patched (Ptch), and smoothened (Smo) expression across different stages of colorectal neoplasia.
Main Methods:
- Immunohistochemistry was used to assess the expression of Shh, Ptch, and Smo.
- The study analyzed 17 hyperplastic polyps, 24 adenomas, 69 adenocarcinomas (well- and moderately-differentiated), and 30 normal colon samples.
Main Results:
- Shh was expressed in 96% of adenomas, 24% of hyperplastic polyps, 23% of well-differentiated adenocarcinomas, and 34% of moderately-differentiated adenocarcinomas.
- No Shh expression was detected in normal colon samples.
- Expression rates of Ptch and Smo increased progressively with tumor progression.
Conclusions:
- Shh expression and Shh-related carcinogenesis may initiate the adenoma-carcinoma sequence in the colon.
- Targeting hedgehog signaling through blockade presents a potential therapeutic strategy for colorectal carcinogenesis.
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