Background: Cytogenetic evaluation is a key component of the diagnosis and prognosis of chronic lymphocytic leukemia (CLL). We performed oligonucleotide-based comparative genomic hybridization microarray analysis on 34 samples with CLL and known abnormal karyotypes previously determined by cytogenetics and/or fluorescence in situ hybridization (FISH).
Results: Using a custom designed microarray that targets >1800 genes involved in hematologic disease and other malignancies, we identified additional cryptic aberrations and novel findings in 59% of cases. These included gains and losses of genes associated with cell cycle regulation, apoptosis and susceptibility loci on 3p21.31, 5q35.2q35.3, 10q23.31q23.33, 11q22.3, and 22q11.23.
Conclusions: Our results show that microarray analysis will detect known aberrations, including microscopic and cryptic alterations. In addition, novel genomic changes will be uncovered that may become important prognostic predictors or treatment targets for CLL in the future.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3253687 | PMC |
| http://dx.doi.org/10.1186/1755-8166-4-25 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Improved Malignancy of Colon Cancer Cells at Gene Expression Level with Constitutive Activation of the Eukaryotic Elongation Factor 2 (eEF2) Under Nutrition Deficient Conditions.
Chem Biodivers
January 2025
Biruni Universitesi, Molecular Biology and Genetics, Biruni Uni, İstanbul, TURKEY.
Regulation of protein production in response to physiological signals is achieved through precise control of Eukaryotic Elongation Factor 2 (eEF2), whose distinct translocase function is crucial for cell survival. Phosphorylation of eEF2 at its Thr56 (T56) residue inactivates this function in translation. Using genetically modified paralogue of a colon cancer cell line, HCT116 which carries a point mutation at Ser595-to-Alanine in the eEF2 gene we were able to create a constitutively active form of eEF2.
View Article and Find Full Text PDFP-, E-, and H-cadherins differ in their relationships with coronary stenosis, cardiovascular outcomes, and unplanned recurrent revascularization.
J Mol Cell Cardiol Plus
September 2024
National Research Center for Preventive Medicine (NRCPM), Petroverigsky, 10, building 3, Moscow 101990, Russia.
Background And Aims: Cadherins are adhesion proteins, and their dysregulation may result in the development of atherosclerosis, plaque rupture, or lesions of the vascular wall. The aim of the present study was to detect the associations of cadherins-P, -E, and -H, with atherosclerosis and pathological cardiovascular conditions.
Methods And Results: The present study with 3-year follow up evaluated atherosclerosis and fasting levels of P-, E-, and H-cadherins in the serum samples of 214 patients in a hospital setting.
Pooled microarray expression analysis of failing left ventricles reveals extensive cellular-level dysregulation independent of age and sex.
J Mol Cell Cardiol Plus
March 2024
National Coalition of Independent Scholars, 125 Putney Road, Battleboro, VT 05301, United States.
Existing cardiovascular studies tend to suffer from small sample sizes and unaddressed confounders. Re-profiling of 9 microarray datasets revealed significant global gene expression differences between 358 failing and 191 non-failing left ventricles independent of age and sex ( = 5.1e-10).
View Article and Find Full Text PDFIdentification of crucial extracellular genes as potential biomarkers in newly diagnosed Type 1 diabetes integrated bioinformatics analysis.
PeerJ
January 2025
Department of Endocrinology, Sir Run Run Hospital, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Purpose: In this study, we aimed to study the role of extracellular proteins as biomarkers associated with newly diagnosed Type 1 diabetes (NT1D) diagnosis and prognosis.
Patients And Methods: We retrieved and analyzed the GSE55098 microarray dataset from the Gene Expression Omnibus (GEO) database. Using R software, we screened out the extracellular protein-differentially expressed genes (EP-DEGs) through several protein-related databases.
In-depth Computational Analysis Reveals The Significant Dysregulation of Key Gap Junction Proteins (GJPs) Driving Thoracic Aortic Aneurysm Development.
Hellenic J Cardiol
January 2025
Department of Cardiac Surgery Research, Lankenau Institute for Medical Research, Main Line Health, Wynnewood, PA, 19096, USA; Department of Cardiac Surgery, Lankenau Heart Institute, Main Line Health, Wynnewood, PA, 19096, USA. Electronic address:
Objective: Thoracic Aortic Aneurysm (TAA) represents an aortic pathology that is caused by the deranged integrity of the three layers of the aortic wall, and is related to severe morbidity and mortality. Consequently, it is crucial to identify the biomarkers implicated in the pathogenesis and biology of TAA. The aim of the current computational study was to assess the differential gene expression profile of the gap junction proteins (GJPs) in patients with TAA in order to identify novel potential biomarkers for the diagnosis and treatment of this disease.
View Article and Find Full Text PDFWant 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!