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Overexpression of p16INK4A as a specific marker for dysplastic and neoplastic epithelial cells of the cervix uteri
Data demonstrate that p16INK4a is a specific biomarker to identify dysplastic cervical epithelia in sections of cervical biopsy samples or cervical smears and that Dysplastic cells could also be identified in cervicalsmears using a specific p16ink4a monoclonal antibody. Expand
Potential of fecal microbiota for early-stage detection of colorectal cancer
CRC‐associated changes in the fecal microbiome at least partially reflected microbial community composition at the tumor itself, indicating that observed gene pool differences may reveal tumor‐related host–microbe interactions. Expand
Detection of high-risk cervical intraepithelial neoplasia and cervical cancer by amplification of transcripts derived from integrated papillomavirus oncogenes.
A protocol for the amplification of papillomavirus oncogene transcripts (APOT) from cervical specimens is established that allows us to distinguish episome- from integrate-derived HPV mRNAs. Expand
Type-dependent integration frequency of human papillomavirus genomes in cervical lesions.
It is suggested that integration of oncogenic HPV genomes in cervical lesions is a consequence rather than the cause of chromosomal instability induced by deregulated HR-HPV E6-E7 oncogene expression. Expand
p16INK4a Immunohistochemistry Improves Interobserver Agreement in the Diagnosis of Cervical Intraepithelial Neoplasia
It has been repeatedly shown that there is a substantial lack of interobserver reproducibility in the histologic diagnosis of cervical intraepithelial neoplasia (CIN), which might be improved by aExpand
Lower incidence of colorectal cancer and later age of disease onset in 27 families with pathogenic MSH6 germline mutations compared with families with MLH1 or MSH2 mutations: the German Hereditary
Later age of disease onset and lower incidence of colorectal cancer may contribute to a lower proportion of identified MSH6 mutations in families suspected of HNPCC, but a surveillance program as stringent as that for families with MLH1 or MSH2 mutations is recommended. Expand
Mutational activation of the beta-catenin proto-oncogene is a common event in the development of Wilms' tumors.
Findings indicate that activating beta-catenin mutations may play a significant role in the development of WTs and establish a direct link between Wilms' tumorigenesis and the Wnt signal transduction pathway governing normal kidney development. Expand
New markers for cervical dysplasia to visualise the genomic chaos created by aberrant oncogenic papillomavirus infections.
D detection of specific viral mRNAs derived from integrated HPV genomes in advanced precancers can be used to identify lesions with a particularly high risk for progression into invasive carcinomas (APOT assay) and will result in a modified classification of cervical precancers and improved screening assays. Expand
Evidence for at least three alternative mechanisms targeting the p16INK4A/cyclin D/Rb pathway in penile carcinoma, one of which is mediated by high‐risk human papillomavirus
There are at least three plausible mechanisms by which the p16INK4A/cyclin D/Rb pathway can become disrupted during penile carcinogenesis, and methylation of the p15ink4A promoter or overexpression of the BMI‐1 polycomb gene product may provide alternative modes of interference with this pathway. Expand
Risks of less common cancers in proven mutation carriers with lynch syndrome.
The sex- and gene-specific differences of less common cancer risks should be taken into account in cancer surveillance and prevention programs for patients with Lynch syndrome. Expand