AI Article Synopsis

Article Abstract

The purpose of the study was to compare cytogenetic profiles and survivals between elderly and non-elderly Chinese patients with diffuse large B-cell lymphoma (DLBCL). We identified 50 patients with DLBCL and divided them by age into elderly (≥60 years) and non-elderly (< 60 years) groups. We detected deletion of P53 or translocations in Bcl-2, Bcl-6 or c-myc genes by fluorescence in situ hybridization (FISH). P53 deletion was significantly more common in elderly versus non-elderly patients (62% vs. 17%, respectively, p=0.001) There were no significant differences in rates of Bcl-2, Bcl-6 or c-myc gene rearrangements between elderly and non-elderly patients (p>0.25 for each). Median survival was significantly longer in non-elderly compared to elderly patients. P53 deletion was an independent prognostic factor for decreased survival in patients with DLBCL, independent of age. In conclusion, P53 deletion as detected by FISH is associated with both increased age and decreased survival in Chinese patients with DLBCL. This association with decreased survival is at least partly independent of age. P53 deletion could serve as a prognostic factor in DLBCL independent of or in combination with age.

Download full-text PDF

Source
http://dx.doi.org/10.3109/10428194.2012.686106DOI Listing

Publication Analysis

Top Keywords

p53 deletion
20
decreased survival
16
chinese patients
12
patients dlbcl
12
associated increased
8
increased age
8
age decreased
8
patients
8
patients diffuse
8
diffuse large
8

Similar Publications

IP6K1 rewires LKB1 signaling to mediate hyperglycemic endothelial senescence.

Diabetes

January 2025

Institute for Developmental and Regenerative Cardiovascular Medicine, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.

Diabetes is a major risk factor for cardiovascular disease, but the molecular mechanisms underlying diabetic vasculopathy have been elusive. Here we report that inositol hexakisphosphate kinase 1 (IP6K1) mediates hyperglycemia-induced endothelial senescence by rewiring the liver kinase B1 (LKB1) signaling from activating the adenosine monophosphate-activated protein kinase (AMPK) pathway to the p53 pathway. We found that hyperglycemia upregulated IP6K1, which disrupts the Hsp/Hsc70 and carboxyl terminus of Hsc70-interacting protein (CHIP)-mediated LKB1 degradation, leading to increased expression levels of LKB1.

View Article and Find Full Text PDF

Wip1 phosphatase activator QGC-8-52 specifically sensitizes p53-negative cancer cells to chemotherapy while protecting normal cells.

Drug Resist Updat

December 2024

Department of Oncology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200123, China. Electronic address:

PP2C serine-threonine phosphatase Wip1 plays an important role in normal tissue homeostasis, stress signaling and pathogenesis of various human diseases. It is an attractive drug target for cancer treatment and inhibition of its expression or activity constitute a novel therapeutic intervention strategy to prevent the development of various cancers. However, previous strategies for Wip1 suppression may be ineffective in cancers lacking p53.

View Article and Find Full Text PDF

Background: Juvenile granulosa cell tumor (JGCT) of the ovary is a rare tumor with distinct clinicopathological and hormonal features primarily affecting young women and children. We conducted a complex clinicopathological, immunohistochemical, and molecular analysis of five cases of JGCT.

Methods: The immunohistochemical examination was performed with 32 markers, including markers that have not been previously investigated.

View Article and Find Full Text PDF

Mutant p53-Mediated Tumor Secretome: Bridging Tumor Cells and Stromal Cells.

Genes (Basel)

December 2024

Laboratory of Molecular Genetics of Aging & Tumor, Medical School, Kunming University of Science and Technology, Chenggong Campus, 727 South Jingming Road, Kunming 650500, China.

The tumor secretome comprises the totality of protein factors secreted by various cell components within the tumor microenvironment, serving as the primary medium for signal transduction between tumor cells and between tumor cells and stromal cells. The deletion or mutation of the gene leads to alterations in cellular secretion characteristics, contributing to the construction of the tumor microenvironment in a cell non-autonomous manner. This review discusses the critical roles of mutant p53 in regulating the tumor secretome to remodel the tumor microenvironment, drive tumor progression, and influence the plasticity of cancer-associated fibroblasts (CAFs) as well as the dynamics of tumor immunity by focusing on both secreted protein expression and secretion pathways.

View Article and Find Full Text PDF

Background: Prostate cancer is the most common diagnosed tumor and the fifth cancer related death among men in Europe. Although several genetic alterations such as ERG-TMPRSS2 fusion, MYC amplification, PTEN deletion and mutations in p53 and BRCA2 genes play a key role in the pathogenesis of prostate cancer, specific gene alteration signature that could distinguish indolent from aggressive prostate cancer or may aid in patient stratification for prognosis and/or clinical management of patients with prostate cancer is still missing. Therefore, here, by a multi-omics approach we describe a prostate cancer carrying the fusion of TMPRSS2 with ERG gene and deletion of 16q chromosome arm.

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!