ArticleBritish journal of haematology2023
Patient-derived xenograft models of ALK+ ALCL reveal preclinical promise for therapy with brigatinib.
Article in British journal of haematology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- CircZBTB46, a promising therapeutic target in crizotinib resistant ALK-positive T lymphomas.Leukemia · 2026Article
- HDAC1 acts as a tumor suppressor in ALK-positive anaplastic large cell lymphoma: implications for HDAC inhibitor therapy.Leukemia · 2025Article
- Pediatric relapsed/refractory ALK-positive anaplastic large cell lymphoma treatment and outcomes in the targeted-drug era.Blood advances · 2025Article
- Enhancing drug penetration in solid tumors via nanomedicine: Evaluation models, strategies and perspectives.Bioactive materials · 2024Review
- Patient-derived xenograft models of ALK+ ALCL reveal preclinical promise for therapy with brigatinib.British journal of haematology · 2023Article
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Authors and funding
14 authors at 8 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anaplastic large-cell lymphoma (ALCL) is a T-cell malignancy predominantly driven by the oncogenic anaplastic lymphoma kinase (ALK), accounting for approximately 15% of all paediatric non-Hodgkin lymphoma. Patients with central nervous system (CNS) relapse are particularly difficult to treat with a 3-year overall survival of 49% and a median survival of 23.5 months. The second-generation ALK inhibitor brigatinib shows superior penetration of the blood-brain barrier unlike the first-generation drug crizotinib and has shown promising results in ALK+ non-small-cell lung cancer. However, the benefits of brigatinib in treating aggressive paediatric ALK+ ALCL are largely unknown. We established a patient-derived xenograft (PDX) resource from ALK+ ALCL patients at or before CNS relapse serving as models to facilitate the development of future therapies. We show in vivo that brigatinib is effective in inducing the remission of PDX models of crizotinib-resistant (ALK C1156Y, TP53 loss) ALCL and furthermore that it is superior to crizotinib as a second-line approach to the treatment of a standard chemotherapy relapsed/refractory ALCL PDX pointing to brigatinib as a future therapeutic option.
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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.