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Updated: Mar 26, 2026

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
Published on: July 28, 2010
The pathological phenotype of colon cancer with microsatellite instability
Helene Schou Andersen1, Claus Anders Bertelsen, Rikke Henriksen
1helene@ksandersen.dk.
Introduction:
Colorectal cancer is a common malignant disease, caused by different aetiologies and molecular pathways. Heterogeneous results have been published regarding the association of microsatellite instability and clinicopathological features. The aim of this study was to compare clinicopathological features of microsatellite unstable tumours with stable ones.
Methods:
Data were collected retrospectively, but the pathological analyses were all made prospectively. The study included a total of 833 patients undergoing resection of their colon tumour at Nordsjællands Hospital - Hillerød, with mismatch repair analysis from 1 January 2007 to 30 November 2012. The study was performed in a setting with complete mesocolic excision surgery and post-operative expert pathological examination of the tumours. Mismatch repair analysis was done by immuno-histochemical staining for the mismatch repair proteins: pMLH1, pMSH2, pMSH6 and pPMS2 for the determination of microsatellite instability. Microsatellite instability was defined as deficient expression of one or more of these proteins.
Results:
Of the 833 patients, 177 had microsatellite instable tumours (21%). Using multivariable logistic regression analysis, we demonstrated that microsatellite unstable cancers were significantly associated with a lower degree of lymph node metastases (odds ratio (OR) = 0.92), distant metastases (OR = 0.33) and tumour budding (OR = 0.41).
Conclusions:
We found that microsatellite unstable tumours show a pathological profile that appears less aggressive than the pathological profile of stable tumours.
Funding:
none.
Trial Registration:
not relevant.
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