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Background/aim: Cell lines serve as valuable models to study altered cellular signaling pathways, to identify mutations in key oncogenic genes, and to test potential antitumor drugs. The Jurkat cell line, for example, has provided important information about various signaling pathways in lymphoblastic leukemia, establishing most of what is currently known about T-cell receptor (TCR) signaling. However, many aspects of the genome modification of this cell line have not yet been analyzed. To identify genes of potential biological and clinical relevance in acute T-lymphoblastic leukemia (T-ALL), we performed an array comparative genomic hybridization (aCGH) approach on the widely used Jurkat cell line and examined the association of the detected copy number alterations (CNAs) with cancer hallmarks and T-ALL pathogenesis.
Materials And Methods: Cells were harvested by using trypsin/EDTA from culture flasks to extract genomic DNA. aCGH experiments were performed on an Agilent microarray platform using the SurePrint G3 Cancer CGH + SNP Microarray 4×180 K. Functional enrichment analysis of all CNAs was performed with the R package g:Profiler2. The association of these alterations with key cancer hallmarks was analyzed using the Cancer Hallmarks web-tool.
Results: Our analysis revealed several novel CNAs, including losses at 5p15.2, 6q27, 10q22.2, 14q11.2, 18q11.2-q12.1, and Xp22.33, as well as gains at 2p11.2, 7p21.2, 7q21.2 and 18p11.32. Genes within these regions were associated with important oncogenic pathways, including 'sustained proliferative signaling', 'tumor suppressor evasion', and 'angiogenesis promotion'.
Conclusion: These findings suggest that Jurkat cells may serve as a valuable model for identifying new targets for cancer research. Further studies are required to confirm the phenotypic implications of these variants, which may open new avenues for exploring the functional impact of these alterations and their potential role in the development of therapies.
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http://dx.doi.org/10.21873/cgp.20539 | DOI Listing |
Front Cell Dev Biol
August 2025
Department of Hepatobiliary Surgery, The First Hospital of Putian City, Chengxiang, Fujian, China.
Background: USP37, a versatile deubiquitinase, plays a pivotal role in numerous cellular functions. Although its involvement in cancer development is well-established, the comprehensive pan-cancer analysis of USP37 remains relatively uncharted.
Methods: RNA sequencing data from both normal and cancerous tissues were retrieved from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases.
Nat Rev Cancer
September 2025
Department of Biochemistry and Molecular Biology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
Somatic mutations in several genes, including key oncogenes and tumour suppressor genes, are present from early life and can accumulate as an individual ages, indicating that the potential for cancer is present and growing throughout life. However, the risk of developing cancer rises sharply after 50-60 years of age, suggesting that the ability of these mutations to undergo clonal expansion and drive cancer development is dependent on the progressive changes in the epigenome and microenvironment that occur during ageing. Epigenetic changes, including DNA methylation and histone modifications, can drive various hallmarks of ageing in precancerous cells, including induction of senescence, the senescence-associated secretory phenotype, genomic instability and reduction of nuclear integrity, metabolic and inflammatory stress responses, stem cell function and differentiation potential, and redox balance.
View Article and Find Full Text PDFFerroptosis, an iron-dependent cell death pathway driven by lipid peroxidation, has emerged as a critical pathophysiological mechanism linking cancer and inflammatory diseases. The seemingly distinct pathologies exhibit shared microenvironmental hallmarks-oxidative stress, immune dysregulation, and metabolic reprogramming-that converge on ferroptosis regulation. This review synthesizes how ferroptosis operates at the intersection of these diseases, acting as both a tumor-suppressive mechanism and a driver of inflammatory tissue damage.
View Article and Find Full Text PDFWorld J Surg Oncol
September 2025
Department of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, No.1 Shuaifuyuan Dongcheng District, Beijing, 100730, China.
Purpose: We reviewed recent advancements in the characterization of intraductal oncocytic papillary neoplasm (IOPN) of the pancreas, with a specific focus on developments in immunohistochemical markers, molecular pathology, and pathogenic mechanisms over the past ten years (2015-2024). Through comprehensive analysis of current literature, we aimed to elucidate the evolving understanding of IOPN's biological behavior and diagnostic features, while identifying potential areas for future research in this distinctive pancreatic neoplasm.
Methods: English-language articles on IOPN were searched from Pubmed from the first report of IOPN of the pancreas in 2015 to 2024.
Inn Med (Heidelb)
September 2025
Comprehensive Cancer Center, Universitätsklinik Würzburg, Würzburg, Deutschland.
Frailty is a common geriatric syndrome in older patients with cancer. It affects prognosis and treatment tolerance in various ways. Frailty and cancer share several common risk factors, which are reflected in the hallmarks of aging.
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