Purpose: Making a clinicopathological diagnosis of dysplasia is crucial. We herein assess the significance of the DNA methyltransferase 3b (DNMT3b) expression as a diagnostic marker of ulcerative colitis (UC)-associated neoplasia.
Methods: Thirty-one patients with long-standing and extensive UC were included in this study. The expression of DNMT3b in non-neoplastic rectal epithelium (non-dysplasia in 31 patients) and colorectal neoplasia (dysplasia in 43 patients and invasive cancer in 34 patients) was determined using immunohistochemistry. The presence of immunoreactive DNMT3b was assessed in the areas with the highest density of cells with positively staining nuclei. DNMT3b was expressed as the percentage of positive cells relative to the total number of cells counted under high power magnification.
Results: The DNMT3b expression in neoplastic rectal epithelium (0.76, range 0.59-0.84) was increased compared to that observed in non-neoplastic epithelium (0.32, range 0.18-0.67, P < 0.001). A ROC curve analysis confirmed 0.68 to be the best diagnostic cut-off value for the DNMT3b expression in neoplastic epithelium (area under the curve = 0.810). The sensitivity of the diagnostic test was 66.2 %, the specificity was 86.7 %, the positive predictive value was 95.7 % and the negative predictive value was 36.1 %. The positive likelihood ratio was 4.98 and the negative likelihood ratio was 0.20. The accuracy was 69.9 %.
Conclusions: An immunohistochemical analysis of the DNMT3b expression was associated with significant improvements in the discrimination of UC-associated neoplastic lesions.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s00595-012-0456-6 | DOI Listing |
J Biol Chem
December 2024
Department of Anatomy, Histology and Embryology, Jinzhou Medical University, Jinzhou, China; Liaoning Key Laboratory of Diabetic Cognitive and Perceptive Dysfunction, Jinzhou Medical University, Jinzhou, China. Electronic address:
The remyelination process within the diabetes mellitus (DM) brain is inhibited, and dynamic interactions between DNA methylation and transcription factors are critical for this process. Repressor element-1 silencing transcription factor (REST) is a major regulator of oligodendrocyte differentiation, and the role of REST on DM remyelination remains to be investigated. Here, we investigated the effects of REST and DNA methylation on DM remyelination and explored the underlying mechanisms.
View Article and Find Full Text PDFAdv Biomed Res
November 2024
Department of Cellular and Molecular Nutrition, Faculty of Nutrition Science and Food Technology, National Nutrition and Food Technology Research Institute, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Background: Acquisition of stem-like properties requires overcoming the epigenetic barrier of differentiation and re-expression of several genes involved in stemness and the cell cycle. DNA methylation is the classic epigenetic mechanism for de/differentiation. The writers and erasers of DNA methylation are not site-specific enzymes for altering specific gene methylation.
View Article and Find Full Text PDFCancer Cell Int
December 2024
Department of Biology, University of Alabama at Birmingham, 3100 East Science Hall, 902 14th Street South, Birmingham, AL, 35294-1170, USA.
Background: Epigenetic phytochemicals are considered as an efficacious and safe alternative to synthetic drugs in drug discovery. In this regard, combinatorial interventions enable simultaneously targeting various neoplastic pathways to eradicate multiple tumorigenic clones. Therefore, we evaluated the effects of the epigenetic-modifying compounds phenethyl isothiocyanate (PEITC) and withaferin A (WA) alone and in combination on cancer hallmarks and miRNome profiles of breast cancer (BC) cells in addition to their impact on multiple epigenetic regulatory pathways.
View Article and Find Full Text PDFCommun Biol
December 2024
Guangzhou Institute of Cancer Research, the Affiliated Cancer Hospital, Guangzhou Medical University; State Key Laboratory of Respiratory Disease, Guangzhou, Guangdong, China.
Inevitable gefitinib resistance is the biggest bottleneck in current treatment and the mechanisms are not fully understood. Here, we observe that PFTK1 (also named CDK14) is significantly enhanced in NSCLC with gefitinib resistance. And the upregulation of PFTK1 is negatively associated with progression-free survival (PFS) in NSCLC patients who receive gefitinib treatment.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Unité Organisation Nucléaire et Oncogenèse, INSERM U993, Institut Pasteur, Université Paris Cité, 75015 Paris, France.
Hepatoblastoma is the most common primary liver malignancy in children, with metabolic reprogramming playing a critical role in its progression due to the liver's intrinsic metabolic functions. Enhanced glycolysis, glutaminolysis, and fatty acid synthesis have been implicated in hepatoblastoma cell proliferation and survival. In this study, we screened for altered overexpression of metabolic enzymes in hepatoblastoma tumors at tissue and single-cell levels, establishing and validating a hepatoblastoma tumor expression metabolic score using machine learning.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!