ArticleLeukemia2009
Gene expression profiling of isolated tumour cells from anaplastic large cell lymphomas: insights into its cellular origin, pathogenesis and relation to Hodgkin lymphoma.
Article in Leukemia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 133 citations in OpenAlex.
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- A loss of the cytosolic branched-chain aminotransferase, BCATc, enhances TImmunometabolism (Cobham, Surrey) · 2026Article
- GANT61 suppresses proliferation and induces apoptosis in ALK-Positive anaplastic large cell lymphoma via modulating the Hh-PIK3IP1-Akt signaling axis.Annals of hematology · 2026Article
- Identification and Validation of BATF3 as a Promising Biomarker Gene for Peripheral T-cell Lymphoma.Current medicinal chemistry · 2026Article
- HDAC1 acts as a tumor suppressor in ALK-positive anaplastic large cell lymphoma: implications for HDAC inhibitor therapy.Leukemia · 2025Article
- Inhibition of choline metabolism in an angioimmunoblastic T-cell lymphoma preclinical model reveals a new metabolic vulnerability as possible target for treatment.Journal of experimental & clinical cancer research : CR · 2024Article
- Amino acid metabolism in health and disease.Signal transduction and targeted therapy · 2023Review
- Aberrant expression of GOLM1 protects ALK+ anaplastic large cell lymphoma from apoptosis by enhancing BCL-XL stability.Blood advances · 2023Article
- The emerging role of the branched chain aminotransferases, BCATc and BCATm, for anti-tumor T-cell immunity.Immunometabolism (Cobham, Surrey) · 2023Review
- Differential molecular programs of cutaneous anaplastic large cell lymphoma and CD30-positive transformed mycosis fungoides.Frontiers in immunology · 2023Article
- NR2F6, a new immune checkpoint that acts as a potential biomarker of immunosuppression and contributes to poor clinical outcome in human glioma.Frontiers in immunology · 2023Article
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- Tissue Expander-associated T Cells: Relevance to Breast Implant-associated Anaplastic Large-cell Lymphoma.Plastic and reconstructive surgery. Global open · 2022Article
- The role of B cells in the development, progression, and treatment of lymphomas and solid tumors.Advances in immunology · 2022Review
- The expression and biological effect of NR2F6 in non-small cell lung cancer.Frontiers in oncology · 2022Article
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- Diagnostic and prognostic value of secreted protein acidic and rich in cysteine in the diffuse large B-cell lymphoma.World journal of clinical cases · 2021Article
- A novel model of alternative NF-κB pathway activation in anaplastic large cell lymphoma.Leukemia · 2021Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 9 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anaplastic large cell lymphoma (ALCL) is a main type of T-cell lymphomas and comprises three distinct entities: systemic anaplastic lymphoma kinase (ALK) positive, systemic ALK(-) and cutaneous ALK(-) ALCL (cALCL). Little is known about their pathogenesis and their cellular origin, and morphological and immunophenotypical overlap exists between ALK(-) ALCL and classical Hodgkin lymphoma (cHL). We conducted gene expression profiling of microdissected lymphoma cells of five ALK(+) and four ALK(-) systemic ALCL, seven cALCL and sixteen cHL, and of eight subsets of normal T and NK cells. The analysis supports a derivation of ALCL from activated T cells, but the lymphoma cells acquired a gene expression pattern hampering an assignment to a CD4(+), CD8(+) or CD30(+) T-cell origin. Indeed, ALCL display a down-modulation of many T-cell characteristic molecules. All ALCL types show significant expression of NFkappaB target genes and upregulation of genes involved in oncogenesis (e.g. EZH2). Surprisingly, few genes are differentially expressed between systemic and cALCL despite their different clinical behaviour, and between ALK(-) ALCL and cHL despite their different cellular origin. ALK(+) ALCL are characterized by expression of genes regulated by pathways constitutively activated by ALK. This study provides multiple novel insights into the molecular biology and pathogenesis of ALCL.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.