The circulating auto-antibodies to p53 protein in the follow-up of lymphoma patients.

Oncol Rep

Department of Medical Oncology, Institute of Oncology, 1000 Ljubljana, Slovenia.

Published: March 2001

Mutant p53 proteins may be targets of the host immune system - consequently a certain proportion of cancer patients (the percentage varies according to the type of cancer) with tumors that carry p53 missense mutations develop circulating p53 antibodies. The present study was aimed at defining the occurrence of circulating antibodies to p53 protein in patients with various types of non-Hodgkin's lymphomas (NHL). Altogether, the sera of 108 cases with various histological types of NHL and of 20 healthy controls were assessed for the presence of antibodies to p53 protein with an ELISA method. In 73 cases of NHL, also the immunohistochemical staining for p53 antigen was performed to make a rough estimation of the frequency of mutational events. The development of autoantibodies to p53 protein was observed in approximately 7% of NHL patients (predominantly in the more aggressive variants of the disease, but also in one case of small lymphocytic lymphoma). This proportion represents roughly one third of the number of patients assessed (immunohistochemically) to carry a missense p53 mutation in their tumors. The autoantibodies to p53 protein can be used as a tumor marker (early appearance, high specificity) in the follow-up of a subset of NHL patients, but, unfortunately, this subset comprises only approximately 7% of NHL patients.

Download full-text PDF

Source

Publication Analysis

Top Keywords

p53 protein
20
nhl patients
12
p53
10
antibodies p53
8
autoantibodies p53
8
patients
7
nhl
6
protein
5
circulating auto-antibodies
4
auto-antibodies p53
4

Similar Publications

High glucose induces renal tubular epithelial cell senescence by inhibiting autophagic flux.

Hum Cell

January 2025

Department of Nephrology, Zhong Da Hospital, Gulou District, No. 87, Dingjiaqiao, Zhongyangmen Street, Nanjing, 210009, Jiangsu, China.

Autophagy, a cellular degradation process involving the formation and clearance of autophagosomes, is mediated by autophagic proteins, such as microtubule-associated protein 1 light chain 3 (LC3) and sequestosome 1 (p62), and modulated by 3-methyladenine (3-MA) as well as chloroquine (CQ). Senescence, characterised by permanent cell cycle arrest, is marked by proteins such as cyclin-dependent kinase inhibitor 1 (p21) and tumour protein 53 (p53). This study aims to investigate the relationship between cell senescence and renal function in diabetic kidney disease (DKD) and the effect of autophagy on high-glucose-induced cell senescence.

View Article and Find Full Text PDF

Delays in mitosis trigger p53-dependent arrest in G1 of the next cell cycle, thus preventing repeated cycles of chromosome instability and aneuploidy. Here we show that MDM2, the p53 ubiquitin ligase, is a key component of the timer mechanism triggering G1 arrest in response to prolonged mitosis. This timer function arises due to the attenuation of protein synthesis in mitosis.

View Article and Find Full Text PDF

DARPin-induced reactivation of p53 in HPV-positive cells.

Nat Struct Mol Biol

January 2025

Institute of Biophysical Chemistry and Center for Biomolecular Magnetic Resonance, Goethe University, Frankfurt, Germany.

Infection of cells with high-risk strains of the human papillomavirus (HPV) causes cancer in various types of epithelial tissue. HPV infections are responsible for ~4.5% of all cancers worldwide.

View Article and Find Full Text PDF

Purpose: This study focused on combining irinotecan with Poly (ADP-ribose) polymerase (PARP) inhibitors to explore the potential for novel combination therapeutics in small cell lung cancer (SCLC).

Materials And Methods: We selected 10 different SCLC cell lines with diverse mutational backgrounds in DNA damage response (DDR) pathway genes to evaluate the efficacy of the combination of three PARP inhibitors and irinotecan. After the cells were exposed to the drugs for seven days, cell viability was measured, and a combination index was calculated.

View Article and Find Full Text PDF

Ubiquitin-specific peptidase 10 promotes renal interstitial fibrosis progression through deubiquitinating and stabilizing P53 protein.

Biochim Biophys Acta Mol Basis Dis

January 2025

Department of Pediatric Nephrology and Rheumatism and Immunology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong 250021, China; Department of Pediatric Nephrology and Rheumatism and Immunology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250021, China. Electronic address:

Renal interstitial fibrosis is the main factor determining chronic kidney disease (CKD) progression, and renal tubular epithelial cells are the key drivers of this pathological process. Herein, we revealed significantly increased ubiquitin-specific peptidase 10 (USP10) expression in the kidney tissues of both patients with CKD and mice induced by unilateral ureteral obstruction, as well as in transforming growth factor-beta 1 (TGFβ1)-induced renal tubular epithelial cells. In vivo, treatment with the USP10 small molecule inhibitor Spautin-1, which inhibits its deubiquitinating activity, weakened renal interstitial fibrosis progression and alleviated the subsequent inflammatory response and oxidative stress in male mice.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!