PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 14685671

[Virtual colonography].

Christoph Vogt·Mathias Cohnen·Andreas Beck·Volker Aurich·Ulrich Mödder·Dieter Häussinger
View original source ↗Export metadata ↓

Abstract

Recent technical developments in computed tomography (CT) and magnetic resonance imaging (MRI) have made a virtual presentation of the colon possible. The results of clinical investigations comparing virtual colonography and conventional colonoscopy up to now are promising. Virtual colonography is a potential tool for colorectal carcinoma screening in the future, but it still has an unsatisfactory sensitivity for the detection of small and flat lesions and exposes the patient to substantial doses of ionizing radiation. Recent investigations using ultra-low-dose (< 2 mSv) multislice CT colonography show promising results. Magnetic resonance (MR) colonography as a radiation-free modality is the technique of the future. Although encouraging results using virtual MR colonography for the detection of colorectal polyps have been reported, the sensitivity of detecting small polyps (</= 10 mm) and flat lesions is poor. Main reason is the limited spatial resolution in MRI of the colon. The potential role of virtual colonography in the prevention of colorectal cancer is not yet clear. Larger studies with asymptomatic persons at average risk are needed, and further improvements in the detection of flat and very small (< 5 mm) lesions need to be achieved before advocating the use of virtual colonography for routine colorectal cancer screening.

Explore related subjects

AdenomaColonic PolypsColonography, Computed TomographicColonoscopyColorectal NeoplasmsContrast MediaDiagnosis, DifferentialHumansImaging, Three-DimensionalMagnetic Resonance ImagingMass ScreeningRadiation DosageResearchSensitivity and SpecificitySigmoid NeoplasmsTomography, Spiral ComputedComparative StudyJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Christoph Vogt, Mathias Cohnen, Andreas Beck, Volker Aurich, Ulrich Mödder, Dieter Häussinger. 2003-12-15. [Virtual colonography].. https://doi.org/10.1007/s00063-003-1316-3

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2009

HMGA proteins up-regulate CCNB2 gene in mouse and human pituitary adenomas.

The high mobility group As (HMGAs) belong to a family of nonhistone nuclear proteins that orchestrate the assembly of nucleoprotein complexes. Through a complex network of protein-DNA and protein-protein interaction, they play important roles in gene transcription, recombination, and chromatin structure. This protein family is involved, through different mechanisms, in both benign and malignant neoplasias. We have recently reported that transgenic mice carrying the Hmga1 or Hmga2 genes under transcriptional control of the cytomegalovirus promoter develop pituitary adenomas secreting prolactin and growth hormone. We have shown that the mechanism of the HMGA2-induced pituitary adenoma is based on the increased E2F1 activity. The expression profile of mouse normal pituitary glands and adenomas induced in HMGA transgenic mice revealed an increased expression of the ccnb2 gene, coding for the cyclin B2 protein, in the neoplastic tissues compared with the normal pituitary gland. Here, we show, by electrophoretic mobility shift assay and chromatin immunoprecipitation, a direct binding of HMGA proteins to the promoter of ccnb2 gene, whereas luciferase assays showed that HMGAs are able to up-regulate ccnb2 promoter activity. Finally, we report an increased CCNB2 expression in human pituitary adenomas of different histotypes that is directly correlated with HMGA1 and HMGA2 expression. Because cyclin B2 is involved in the regulation of the cell cycle, these results taken together indicate that HMGA-induced cyclin B2 overexpression gives an important contribution to experimental and human pituitary tumorigenesis.

Adenoma↗
PubMed2007

A hierarchical non-homogenous Poisson model for meta-analysis of adenoma counts.

We use a hierarchical model for a meta-analysis that combines information from autopsy studies of adenoma prevalence and counts. The studies we included reported findings using a variety of adenoma prevalence groupings and age categories. We use a non-homogeneous Poisson model for multinomial bin probabilities. The Poisson model allows risk to depend on age and sex, and incorporates extra-Poisson variability. We evaluate model fit using the posterior predicted distribution of adenoma prevalence reported by the studies included in our analyses and validate our model using adenoma prevalence reported by more recent colonoscopy studies. For 1990, the estimated adenoma prevalence among Americans at age 60 is 40.3 per cent for men compared to 29.2 per cent for women.

Adenoma↗
PubMed2006

Diet, lifestyle and risk of K-ras mutation-positive and -negative colorectal adenomas.

K-ras mutation-positive (K-ras+) and -negative (K-ras-) colorectal adenomas may differ clinically and pathologically. As environmental compounds may cause mutations in the growth-related K-ras oncogene or affect clonal selection depending on mutational status, we evaluated whether the aetiology of K-ras+ and K-ras- adenomas differs. K-ras mutations in codons 12 and 13 were assessed in colorectal adenoma tissue (K-ras+: n = 81, K-ras-: n = 453). Dietary and lifestyle data were collected through questionnaires that were also administered to 709 polyp-free controls. Multiple logistic regression analyses showed that intake of vitamin B2 and monounsaturated fat were differently associated with risk of K-ras+ and K-ras- adenomas; vitamin B2 was inversely associated with K-ras- (highest vs. lowest tertile: odds ratio (OR) = 0.70, 95% confidence interval (CI) = 0.50-0.97, p trend = 0.020), but not with K-ras+ adenomas, and a positive association with monounsaturated fat was confined to K-ras- adenomas (OR = 1.57, 95% CI = 1.06-2.34, p trend = 0.029). Besides, potential, not statistically significant, differences in risk arose because red meat was distinctly positively associated with K-ras+ adenomas (OR = 1.70, 95% CI = 0.94-3.09, p trend = 0.061); total dietary and polyunsaturated fat tended to be inversely associated with risk of K-ras+ but not of K-ras- adenomas; inverse associations with dairy products, calcium, protein and tea were confined to K-ras- adenomas, and smoking was more markedly positively associated with K-ras- adenomas. No differences in risk of K-ras+ and K-ras- adenomas could be detected for other factors. In conclusion, dietary and lifestyle factors may influence risk of K-ras+ and K-ras- adenomas differently. However, epidemiological literature on diet, lifestyle and colorectal K-ras mutations is inconsistent.

Adenoma↗