Trial reportBlood2015
Tumor-specific HSP90 inhibition as a therapeutic approach in JAK-mutant acute lymphoblastic leukemias.
Trial report in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 40 citations in OpenAlex.
- Bridging the Gap: Cost-Effective Strategies for Detecting Ph-Like B-Lineage ALL in Resource-Limited Settings.Molecular diagnosis & therapy · 2025Review
- PU-H71 (NSC 750424): a molecular masterpiece that targets HSP90 in cancer and beyond.Frontiers in pharmacology · 2024Review
- Co-targeting HSP90 alpha and CDK7 overcomes resistance against HSP90 inhibitors in BCR-ABL1+ leukemia cells.Cell death & disease · 2023Article
- The role of ruxolitinib treatment in JAK-mutated Ph-like acute lymphoblastic leukemia.Annals of hematology · 2023Article
- Article
- Exploring the oncogenic and therapeutic target potential of the MYB-TYK2 fusion gene in B-cell acute lymphoblastic leukemia.Cancer gene therapy · 2022Article
- Inhibition of adult T-cell leukemia cell proliferation by polymerized proanthocyanidin from blueberry leaves through JAK proteolysis.Cancer science · 2022Article
- The penalty of stress - Epichaperomes negatively reshaping the brain in neurodegenerative disorders.Journal of neurochemistry · 2021Review
- Integrative proteomics reveals the role of E3 ubiquitin ligase SYVN1 in hepatocellular carcinoma metastasis.Cancer communications (London, England) · 2021Article
- Chemical tools for epichaperome-mediated interactome dysfunctions of the central nervous system.Nature communications · 2021Article
- CXCR4 allows T cell acute lymphoblastic leukemia to escape from JAK1/2 and BCL2 inhibition through CNS infiltration.Leukemia & lymphoma · 2021Article
- First-in-Human Trial of Epichaperome-Targeted PET in Patients with Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- The Current Genomic and Molecular Landscape of Philadelphia-like Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2020Review
- Chaperome Networks - Redundancy and Implications for Cancer Treatment.Advances in experimental medicine and biology · 2020Review
- Genetic variants and clinical significance of pediatric acute lymphoblastic leukemia.Annals of translational medicine · 2019Article
- Chaperome heterogeneity and its implications for cancer study and treatment.The Journal of biological chemistry · 2019Review
- Adapting to stress - chaperome networks in cancer.Nature reviews. Cancer · 2018Review
- Article
- Proteomic interrogation of HSP90 and insights for medical research.Expert review of proteomics · 2017Review
- [Research progress in Ph-like childhood acute lymphoblastic leukemia].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
25 authors at 8 institutions in 2 countries.
Funding
Abstract
The development of the dual Janus kinase 1/2 (JAK1/2) inhibitor ruxolitinib for the treatment of myeloproliferative neoplasms (MPNs) has led to studies of ruxolitinib in other clinical contexts, including JAK-mutated acute lymphoblastic leukemia (ALL). However, the limited ability of JAK inhibition to induce molecular or clinicopathological responses in MPNs suggests a need for development of better therapies for JAK kinase-dependent malignancies. Here, we demonstrate that heat shock protein 90 (HSP90) inhibition using a purine-scaffold HSP90 inhibitor in early clinical development is an effective therapeutic approach in JAK-dependent ALL and can overcome persistence to JAK-inhibitor therapy in ALL cells.
Indexed as
Identifiers
What OpenQuestion holds
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.