2023
DOI: 10.1007/s12185-023-03537-7
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Mature T-cell and NK-cell lymphomas: updates on molecular genetic features

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Cited by 4 publications
(3 citation statements)
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“…26 The constitutively activated ALK drives cell proliferation and inhibits apoptosis through activation of signaling pathways (including JAK/STAT, PI3K/AKT), and promotes immune evasion via STAT3-mediated PD-L1 expression. 27 Genomic studies of ALK+ ALCL have also reported mutations in TP53 (11%), as well as in genes involved in epigenetic modification (EP300, KMT2D), TCR signaling, and NOTCH1 pathways. 28,29 In particular, NOTCH pathway activation represents a second-line therapeutic target, as suppression of NOTCH1 expression with γ-secretase inhibitors led to apoptosis in ALK inhibitor-resistant ALCL cell lines.…”
Section: Alk+ Alclmentioning
confidence: 99%
See 1 more Smart Citation
“…26 The constitutively activated ALK drives cell proliferation and inhibits apoptosis through activation of signaling pathways (including JAK/STAT, PI3K/AKT), and promotes immune evasion via STAT3-mediated PD-L1 expression. 27 Genomic studies of ALK+ ALCL have also reported mutations in TP53 (11%), as well as in genes involved in epigenetic modification (EP300, KMT2D), TCR signaling, and NOTCH1 pathways. 28,29 In particular, NOTCH pathway activation represents a second-line therapeutic target, as suppression of NOTCH1 expression with γ-secretase inhibitors led to apoptosis in ALK inhibitor-resistant ALCL cell lines.…”
Section: Alk+ Alclmentioning
confidence: 99%
“…The most common chromosomal translocation is t (2, 5) that partners ALK on chromosome 2 with NPM1 resulting in a constitutively active kinase 26 . The constitutively activated ALK drives cell proliferation and inhibits apoptosis through activation of signaling pathways (including JAK/STAT, PI3K/AKT), and promotes immune evasion via STAT3‐mediated PD‐L1 expression 27 . Genomic studies of ALK+ ALCL have also reported mutations in TP53 (11%), as well as in genes involved in epigenetic modification ( EP300 , KMT2D ), TCR signaling, and NOTCH1 pathways 28,29 .…”
Section: Molecular Pathogenesis Of Ptcl Subtypesmentioning
confidence: 99%
“…Extranodal entities, as detailed by Lewis, Zhou and Dogan, 22 with a clinical lens provided by Stuver, Epstein-Peterson and Horwitz, 23 are identified by their primary location. They constitute a diverse and rare group of diseases with a limited number of dedicated clinical trials, making therapeutic advancement very challenging.…”
mentioning
confidence: 99%