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ProteomicsArsenic Trioxide Acts as a Molecular Glue to Promote STUB1-Mediated NPM-ALK Degradation in ALK⁺ ALCL
The NPM-ALK fusion constitutively activates ALK tyrosine kinase, driving oncogenesis in anaplastic large cell lymphoma (ALCL). Although arsenic trioxide (ATO) exhibits therapeutic potential in NPM-ALK⁺ ALCL by inhibiting proliferation and inducing apoptosis, its molecular mechanism remains unclear. ...
ORGANISM(S): Homo sapiens (Human) 
2026-09-07 | PXD073992 | Pride
Deslanoside Ato Targeted protein degradation Npm-alk+ alcl Stub1 Combination therapy 
ProteomicsArsenic Trioxide Acts as a Molecular Glue to Promote STUB1-Mediated NPM-ALK Degradation in ALK⁺ ALCL
The NPM-ALK fusion constitutively activates ALK tyrosine kinase, driving oncogenesis in anaplastic large cell lymphoma (ALCL). Although arsenic trioxide (ATO) exhibits therapeutic potential in NPM-ALK⁺ ALCL by inhibiting proliferation and inducing apoptosis, its molecular mechanism remains unclear. ...
ORGANISM(S): Homo sapiens (Human) 
2026-09-07 | PXD074054 | Pride
Karpas299 Ato Targeted protein degradation Npm-alk+ alcl 
TranscriptomicsTranscription profiling of human anaplastic large cell lymphoma cell lines - kinase signature
Anaplastic Large Cell Lymphomas (ALCL) represent a subset of lymphomas in which the Anaplastic Lymphoma Kinase (ALK) gene is frequently fused to the NPM gene. We previously demonstrated that the constitutive phosphorylation of ALK chimeric proteins is sufficient to induce cellular transformation in ...
ORGANISM(S): Homo sapiens 
2008-06-14 | E-GEOD-6184 | biostudies-arrayexpress
UnknownBRG1 and NPM-ALK Are Co-Regulated in Anaplastic Large-Cell Lymphoma; BRG1 Is a Potential Therapeutic Target in ALCL.
Not available
S-EPMC8750310 | biostudies-literature
UnknownDe novo generation of the NPM-ALK fusion recapitulates the pleiotropic phenotypes of ALK+ ALCL pathogenesis and reveals the ROR2 receptor as target for tumor cells.
Not available
S-EPMC8895835 | biostudies-literature
UnknownEBP2, a novel NPM-ALK-interacting protein in the nucleolus, contributes to the proliferation of ALCL cells by regulating tumor suppressor p53.
Not available
S-EPMC7782078 | biostudies-literature
TranscriptomicsNPM-ALK expression levels identify two distinct signatures in Anaplastic Large Cell Lymphoma of Childhood
Anaplastic large-cell lymphoma (ALCL) makes up approximately 15% of paediatric non-Hodgkin's lymphomas of childhood. The vast majority of them is associated with the t(2;5)(p23;q35) translocation that results in the expression of a hybrid oncogenic tyrosine kinase, NPM-ALK. In order to investigate A...
ORGANISM(S): Homo sapiens 
2016-11-04 | GSE78513 | GEO
UnknownNIPA (Nuclear Interaction Partner of ALK) Is Crucial for Effective NPM-ALK Mediated Lymphomagenesis.
Not available
S-EPMC9137267 | biostudies-literature
UnknownNPM-ALK Is a Key Regulator of the Oncoprotein FOXM1 in ALK-Positive Anaplastic Large Cell Lymphoma.
Not available
S-EPMC6721812 | biostudies-literature
TranscriptomicsTranscription profiling of 32 human Anaplastic Large Cell Lymphomas (ALCL) and 5 ALCL cell lines to investigate differences between tumors expressing/not-expressing Anaplastic Lymphoma kinkase
A "Cartes d'Identite des Tumeurs" (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net). Affymetrix UU133A gene expression data for a series of 32 cases of systemic Anaplastic Large Cell Lymphoma
(ALCL) and 5 ALCL cell lines; used to (1) confirm that tumors...
ORGANISM(S): Homo sapiens 
2007-05-05 | E-TABM-117 | biostudies-arrayexpress
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