To investigate the expression of p16(INK4a) in cervical carcinoma and its relation to the transition of carcinoma in situ to invasive carcinoma, and its role in recurrence of cervical lesions as well, a series of 90 patients with cervical carcinoma (49 with in situ lesion and 41 with invasive lesion) were selected from July 2001 and September 2002. Groups with in situ and invasive lesions were paired for a series of risk variables for cervical cancer and followed up for 60 months. The follow-up visits occurred every 6 months in the first three years and annually up to the fifth year. It was observed that 87.9% of the patients with invasive lesion showed overexpression of p16(INK4a), in comparison with 37.6% of those with in situ lesion (X(2): 13.68; 2 df; p=0.0002; OR: 12.08), demonstrating overexpression of p16(INK4a) as a risk of invasion of the basal layer by dysplastic cells. We also observed an association between overexpression of p16(INK4a) and staging of cancer (X(2): 18.38; 6 df; p=0.0003). A prospective analysis, when controlled for interaction with cervical lesion groups (by Cox regression), demonstrated a risk of recurrence of 4.83 times attributed to overexpression of p16(INK4a), albeit not statistically significant (p=0.14).
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http://dx.doi.org/10.1016/j.yexmp.2008.11.006 | DOI Listing |
Aging Cell
December 2024
Department of Nanomedicine, Houston Methodist Research Institute, Houston, Texas, USA.
Mesenchymal stem cells (MSCs) are promising candidates for regenerative therapies due to their self-renewal and differentiation capabilities. Pathological microenvironments expose MSCs to senescence-inducing factors such as reactive oxygen species (ROS), resulting in MSC functional decline and loss of stemness. Oxidative stress leads to mitochondrial dysfunction, a hallmark of senescence, and is prevalent in aging tissues characterized by elevated ROS levels.
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November 2024
CNRS, INSERM, iBV, Université Côte d'Azur, 06107 Nice, France.
P16Ink4a is a well-established marker of senescence. Although P16Ink4a is expressed in endothelial cells, little is known about its function in these cells. Using isolated liver endothelial cells with silencing or overexpression of P16Ink4a, we show here that dependent on P16Ink4a levels, different pathways and functions are affected.
View Article and Find Full Text PDFBMC Gastroenterol
December 2024
Human Genetics Unit, Indian Statistical Institute, 203, B. T. Road, Kolkata, 700108, India.
Background And Introduction: Two and half percent of the Indian population suffer from gallbladder cancer (GBC). The primary factors that lead GBC are associated with mutation of several protooncogenes such as EGFR, ERBB2, Myc, and CCND1 along with dysregulation of several tumor suppressor genes such as SMAD4 and CDKN2A. Bacterial infection caused by S.
View Article and Find Full Text PDFInt J Mol Sci
November 2024
Laboratory of Metabolic Manipulation of Herbivorous Animal Nutrition, College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.
The circadian gene is recognized for its regulatory effects on cell proliferation and lipid metabolism across various non-ruminant cells. This study investigates the influence of gene overexpression on goat rumen epithelial cells using a constructed pcDNA3.1- plasmid, assessing its impact on circadian gene expression, cell proliferation, and mRNA levels of short-chain fatty acid (SCFA) transporters, alongside genes related to lipid metabolism, cell proliferation, and apoptosis.
View Article and Find Full Text PDFSci Rep
November 2024
Department of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, Nagasaki University, 1-12-4 Sakamoto, Nagasaki, 852-8523, Japan.
A subset of oropharyngeal squamous cell carcinoma (OPSCC) is caused by the high-risk human papilloma virus (HPV), which expresses p16 immunoreactivity. Dual-color immunofluorescence (IF) analysis of TP53 binding protein-1 (53BP1) and a proliferative indicator, Ki-67, to elucidate genomic instability (GIN) in tumor tissues revealed that abnormal 53BP1 expression is closely associated with carcinogenesis in diverse organs. We have previously demonstrated that the number of 53BP1 nuclear foci (NF) in cervical cells increases with cancer progression.
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