We have previously shown that ICAM-1-deficient mice were resistant to lymphoma dissemination of intravenously injected 164T2 lymphoma cells. Highly aggressive variants of this cell line, however, could overcome this resistance. To discern the complex pattern of gene expression involved in the evolution of aggressiveness in lymphoma cells, we compared the transcriptome of 164T2 cells with that of their aggressive variants using cDNA arrays. We identified several genes that were differentially expressed in nonmetastatic lymphoma cells and their metastatic variants. Galectin-7, associated with the development of chemically induced mammary carcinoma, was one such gene whose expression was significantly upregulated. We showed that it was constitutively expressed in aggressive variants, at both mRNA and protein levels. Galectin-7 expression in aggressive lymphoma cells was induced upon in vivo selection in several organs, including the thymus, the spleen and kidneys. We also showed that treatment of nonaggressive lymphoma cells with 5-aza-2'-deoxycytidine was sufficient to induce galectin-7 gene expression. This report is the first to show that galectin-7 is expressed in aggressive lymphoma.
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http://dx.doi.org/10.1038/sj.leu.2402870 | DOI Listing |
Transl Lung Cancer Res
December 2024
Department of General Thoracic Surgery, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Background: Perioperative treatment of locally advanced non-small cell lung cancer (NSCLC) is attracting attention. The effect of neoadjuvant tyrosine kinase inhibitor (TKI) therapy on postoperative long-term outcomes in patients with driver gene mutations remains unclear. The aim of this study was to clarify the long-term survival outcomes of patients with stage III NSCLC harboring driver gene mutations who received preoperative TKI therapy.
View Article and Find Full Text PDFTransl Lung Cancer Res
December 2024
Department of Pathology, Molecular Pathology Research Center, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China.
Background: The tumor immune microenvironment of anaplastic lymphoma kinase (ALK)-rearranged lung adenocarcinoma (LUAD) stratified by ALK fusion variants is poorly pictured. Hence, in this study, we aim to explore the immune heterogeneity of ALK LUAD across different ALK fusion variants and further investigate their significance on clinical prognosis.
Methods: A retrospective analysis was conducted on ALK LUAD patients (N=68).
Cureus
December 2024
Internal Medicine/Nephrology, Riverside Health System, Yonkers, USA.
We report an interesting case of an elderly male patient with splenic marginal zone lymphoma with a monoclonal cluster of differentiation (CD)5+ B cells. The patient developed signs of renal injury and was evaluated via serum protein electrophoresis and immunofixation electrophoresis, which revealed monoclonal gammopathy with elevated free lambda light chain. However, a bone biopsy ruled out a diagnosis of multiple myeloma.
View Article and Find Full Text PDFHematology
December 2025
Department of Pediatrics, Peking University First Hospital Ningxia Women and Children's Hospital (Ningxia Hui Autonomous Region Maternal and Child Health Hospital), Yinchuan, People's Republic of China.
Background: This study aimed to develop a prognostic model based on extracellular trap-related genes (NETRGs) for patients with cALL.
Methods: Data from the TARGET-ALL-P2 and TARGET-ALL-P3 cohorts in the Genomic Data Commons database, the transcriptome dataset GSE26713, the single-cell transcriptome dataset GSE130116 from the Gene Expression Omnibus database and 306 NETRGs identified were analysed. Differentially expressed genes (DEGs) were identified from GSE26713 and differentially expressed NETRGs (DE-NETRGs) were obtained by overlapping DEGs with NETRGs.
J Biochem Mol Toxicol
February 2025
Department of Neurosurgery, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Objective: Gliomas are the predominant form of malignant brain tumors. We investigated the mechanism of hypoxia-inducible factor-1α (HIF-1α) affecting glioma metabolic reprogramming, proliferation and invasion.
Methods: Human glioma cell U87 was cultured under hypoxia and treated with small interfering (si)HIF-1α, si-B cell lymphoma-2/adenovirus E1B 19-kDa interacting protein 3 (siBNIP3), si-YT521-B homology domain 2 (siYTHDF2), 3-methyladenine and 2-deoxyglucose, with exogenous sodium lactate-treated normally-cultured cells as a lactate-positive control.
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