ArticleBlood2006
Ablation of oncogenic ALK is a viable therapeutic approach for anaplastic large-cell lymphomas.
Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
60 citing papers in PubMed, 128 citations in OpenAlex.
- Fusion genes in cancers: Biogenesis, functions, and therapeutic implications.Genes & diseases · 2025Review
- Tyrosine kinases in nodal peripheral T-cell lymphomas.Frontiers in oncology · 2023Review
- Tyrosine phosphatases regulate resistance to ALK inhibitors in ALK+ anaplastic large cell lymphoma.Blood · 2022Article
- Aberrant expression and genetic alteration of c-MYC in anaplastic large cell lymphoma.Journal of cancer research and clinical oncology · 2022Article
- Regulation of CD45 phosphatase by oncogenic ALK in anaplastic large cell lymphoma.Frontiers in oncology · 2022Article
- BRG1 and NPM-ALK Are Co-Regulated in Anaplastic Large-Cell Lymphoma; BRG1 Is a Potential Therapeutic Target in ALCL.Cancers · 2021Article
- Article
- KRCA-0008 suppresses ALK-positive anaplastic large-cell lymphoma growth.Investigational new drugs · 2020Article
- Article
- Decreased Hepatocyte Autophagy Leads to Synergistic IL-1β and TNF Mouse Liver Injury and Inflammation.Hepatology (Baltimore, Md.) · 2020Article
- pH-responsive DNA nanomicelles for chemo-gene synergetic therapy of anaplastic large cell lymphoma.Theranostics · 2020Article
- Review
- ALK phosphorylates SMAD4 on tyrosine to disable TGF-β tumour suppressor functions.Nature cell biology · 2019Article
- Oligonucleotide Aptamer-Mediated Precision Therapy of Hematological Malignancies.Molecular therapy. Nucleic acids · 2018Review
- Epitope mapping of spontaneous autoantibodies to anaplastic lymphoma kinase (ALK) in non-small cell lung cancer.Oncotarget · 2017Article
- The heterogeneous landscape of ALK negative ALCL.Oncotarget · 2017Review
- Anaplastic large cell lymphoma: pathology, genetics, and clinical aspects.Journal of clinical and experimental hematopathology : JCEH · 2017Review
- Article
- Excess of NPM-ALK oncogenic signaling promotes cellular apoptosis and drug dependency.Oncogene · 2016Article
- Prevalence and clinicopathological characteristics of ALK fusion subtypes in lung adenocarcinomas from Chinese populations.Journal of cancer research and clinical oncology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Anaplastic large-cell lymphomas (ALCLs) carry chromosome translocations in which the anaplastic lymphoma kinase (ALK) gene is fused to several partners, most frequently, the NPM1 gene. We have demonstrated that the constitutive activation of ALK fusion proteins results in cellular transformation and lymphoid neoplasia. Herein, we specifically down-regulated ALK protein expression by using small hairpin RNA (shRNA) targeting a sequence coding for the catalytic domain of ALK. The ablation of ALK leads to the down-modulation of known ALK downstream effectors, cell growth arrest, and reversion of the transformed phenotype of ALK(+) mouse embryonic fibroblasts in vitro and in vivo. In human ALCL cells lentiviral-mediated ALK knock-down leads to G(1) cell-cycle arrest and apoptosis in vitro and tumor growth inhibition and regression in vivo. Using a specific approach we have demonstrated that the survival and growth of ALK(+) ALCLs are strictly dependent on ALK activation and signaling. Therefore, ALK is a viable target for therapeutic intervention and its inactivation might represent a pivotal approach for the treatment of ALK lymphomas and other ALK-dependent human tumors.
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Registered trials
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.